[{"author":[{"full_name":"Morri, Maurizio","last_name":"Morri","id":"4863116E-F248-11E8-B48F-1D18A9856A87","first_name":"Maurizio"},{"last_name":"Sanchez-Romero","full_name":"Sanchez-Romero, Inmaculada","first_name":"Inmaculada","id":"3D9C5D30-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Tichy","full_name":"Tichy, Alexandra-Madelaine","id":"29D8BB2C-F248-11E8-B48F-1D18A9856A87","first_name":"Alexandra-Madelaine"},{"last_name":"Kainrath","full_name":"Kainrath, Stephanie","id":"32CFBA64-F248-11E8-B48F-1D18A9856A87","first_name":"Stephanie"},{"first_name":"Elliot J.","full_name":"Gerrard, Elliot J.","last_name":"Gerrard"},{"full_name":"Hirschfeld, Priscila","last_name":"Hirschfeld","id":"435ACB3A-F248-11E8-B48F-1D18A9856A87","first_name":"Priscila"},{"first_name":"Jan","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","last_name":"Schwarz","full_name":"Schwarz, Jan"},{"id":"33BA6C30-F248-11E8-B48F-1D18A9856A87","first_name":"Harald L","orcid":"0000-0002-8023-9315","full_name":"Janovjak, Harald L","last_name":"Janovjak"}],"external_id":{"isi":["000432280000006"]},"article_processing_charge":"No","title":"Optical functionalization of human class A orphan G-protein-coupled receptors","citation":{"mla":"Morri, Maurizio, et al. “Optical Functionalization of Human Class A Orphan G-Protein-Coupled Receptors.” Nature Communications, vol. 9, no. 1, 1950, Springer Nature, 2018, doi:10.1038/s41467-018-04342-1.","ama":"Morri M, Sanchez-Romero I, Tichy A-M, et al. Optical functionalization of human class A orphan G-protein-coupled receptors. Nature Communications. 2018;9(1). doi:10.1038/s41467-018-04342-1","apa":"Morri, M., Sanchez-Romero, I., Tichy, A.-M., Kainrath, S., Gerrard, E. J., Hirschfeld, P., … Janovjak, H. L. (2018). Optical functionalization of human class A orphan G-protein-coupled receptors. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-018-04342-1","ieee":"M. Morri et al., “Optical functionalization of human class A orphan G-protein-coupled receptors,” Nature Communications, vol. 9, no. 1. Springer Nature, 2018.","short":"M. Morri, I. Sanchez-Romero, A.-M. Tichy, S. Kainrath, E.J. Gerrard, P. Hirschfeld, J. Schwarz, H.L. Janovjak, Nature Communications 9 (2018).","chicago":"Morri, Maurizio, Inmaculada Sanchez-Romero, Alexandra-Madelaine Tichy, Stephanie Kainrath, Elliot J. Gerrard, Priscila Hirschfeld, Jan Schwarz, and Harald L Janovjak. “Optical Functionalization of Human Class A Orphan G-Protein-Coupled Receptors.” Nature Communications. Springer Nature, 2018. https://doi.org/10.1038/s41467-018-04342-1.","ista":"Morri M, Sanchez-Romero I, Tichy A-M, Kainrath S, Gerrard EJ, Hirschfeld P, Schwarz J, Janovjak HL. 2018. Optical functionalization of human class A orphan G-protein-coupled receptors. Nature Communications. 9(1), 1950."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","project":[{"_id":"25548C20-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","grant_number":"303564","name":"Microbial Ion Channels for Synthetic Neurobiology"},{"name":"Molecular Drug Targets","grant_number":"W1232-B24","call_identifier":"FWF","_id":"255A6082-B435-11E9-9278-68D0E5697425"}],"article_number":"1950","doi":"10.1038/s41467-018-04342-1","date_published":"2018-12-01T00:00:00Z","date_created":"2019-02-14T10:50:24Z","isi":1,"has_accepted_license":"1","year":"2018","day":"01","publication":"Nature Communications","publisher":"Springer Nature","quality_controlled":"1","oa":1,"department":[{"_id":"HaJa"},{"_id":"CaGu"},{"_id":"MiSi"}],"file_date_updated":"2020-07-14T12:47:14Z","date_updated":"2023-09-19T14:29:32Z","ddc":["570"],"type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","_id":"5984","volume":9,"issue":"1","ec_funded":1,"publication_identifier":{"issn":["2041-1723"]},"publication_status":"published","file":[{"file_name":"2018_Springer_Morri.pdf","date_created":"2019-02-14T10:58:29Z","file_size":1349914,"date_updated":"2020-07-14T12:47:14Z","creator":"kschuh","file_id":"5985","checksum":"8325fcc194264af4749e662a73bf66b5","content_type":"application/pdf","relation":"main_file","access_level":"open_access"}],"language":[{"iso":"eng"}],"scopus_import":"1","month":"12","intvolume":" 9","abstract":[{"text":"G-protein-coupled receptors (GPCRs) form the largest receptor family, relay environmental stimuli to changes in cell behavior and represent prime drug targets. Many GPCRs are classified as orphan receptors because of the limited knowledge on their ligands and coupling to cellular signaling machineries. Here, we engineer a library of 63 chimeric receptors that contain the signaling domains of human orphan and understudied GPCRs functionally linked to the light-sensing domain of rhodopsin. Upon stimulation with visible light, we identify activation of canonical cell signaling pathways, including cAMP-, Ca2+-, MAPK/ERK-, and Rho-dependent pathways, downstream of the engineered receptors. For the human pseudogene GPR33, we resurrect a signaling function that supports its hypothesized role as a pathogen entry site. These results demonstrate that substituting unknown chemical activators with a light switch can reveal information about protein function and provide an optically controlled protein library for exploring the physiology and therapeutic potential of understudied GPCRs.","lang":"eng"}],"oa_version":"Published Version"},{"title":"On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility","author":[{"first_name":"Setareh","last_name":"Dolati","full_name":"Dolati, Setareh"},{"first_name":"Frieda","full_name":"Kage, Frieda","last_name":"Kage"},{"full_name":"Mueller, Jan","last_name":"Mueller","first_name":"Jan"},{"full_name":"Müsken, Mathias","last_name":"Müsken","first_name":"Mathias"},{"first_name":"Marieluise","full_name":"Kirchner, Marieluise","last_name":"Kirchner"},{"first_name":"Gunnar","full_name":"Dittmar, Gunnar","last_name":"Dittmar"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt"},{"first_name":"Klemens","full_name":"Rottner, Klemens","last_name":"Rottner"},{"first_name":"Martin","full_name":"Falcke, Martin","last_name":"Falcke"}],"article_processing_charge":"No","external_id":{"pmid":["30156465"],"isi":["000455641000011"]},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"mla":"Dolati, Setareh, et al. “On the Relation between Filament Density, Force Generation, and Protrusion Rate in Mesenchymal Cell Motility.” Molecular Biology of the Cell, vol. 29, no. 22, American Society for Cell Biology , 2018, pp. 2674–86, doi:10.1091/mbc.e18-02-0082.","ama":"Dolati S, Kage F, Mueller J, et al. On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility. Molecular Biology of the Cell. 2018;29(22):2674-2686. doi:10.1091/mbc.e18-02-0082","apa":"Dolati, S., Kage, F., Mueller, J., Müsken, M., Kirchner, M., Dittmar, G., … Falcke, M. (2018). On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility. Molecular Biology of the Cell. American Society for Cell Biology . https://doi.org/10.1091/mbc.e18-02-0082","ieee":"S. Dolati et al., “On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility,” Molecular Biology of the Cell, vol. 29, no. 22. American Society for Cell Biology , pp. 2674–2686, 2018.","short":"S. Dolati, F. Kage, J. Mueller, M. Müsken, M. Kirchner, G. Dittmar, M.K. Sixt, K. Rottner, M. Falcke, Molecular Biology of the Cell 29 (2018) 2674–2686.","chicago":"Dolati, Setareh, Frieda Kage, Jan Mueller, Mathias Müsken, Marieluise Kirchner, Gunnar Dittmar, Michael K Sixt, Klemens Rottner, and Martin Falcke. “On the Relation between Filament Density, Force Generation, and Protrusion Rate in Mesenchymal Cell Motility.” Molecular Biology of the Cell. American Society for Cell Biology , 2018. https://doi.org/10.1091/mbc.e18-02-0082.","ista":"Dolati S, Kage F, Mueller J, Müsken M, Kirchner M, Dittmar G, Sixt MK, Rottner K, Falcke M. 2018. On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility. Molecular Biology of the Cell. 29(22), 2674–2686."},"quality_controlled":"1","publisher":"American Society for Cell Biology ","oa":1,"date_published":"2018-11-01T00:00:00Z","doi":"10.1091/mbc.e18-02-0082","date_created":"2019-02-14T12:25:47Z","page":"2674-2686","day":"01","publication":"Molecular Biology of the Cell","has_accepted_license":"1","isi":1,"year":"2018","status":"public","type":"journal_article","tmp":{"name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","image":"/images/cc_by_nc_sa.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","short":"CC BY-NC-SA (4.0)"},"_id":"5992","department":[{"_id":"MiSi"}],"file_date_updated":"2020-07-14T12:47:15Z","ddc":["570"],"date_updated":"2023-09-19T14:30:23Z","month":"11","intvolume":" 29","scopus_import":"1","pmid":1,"oa_version":"Published Version","abstract":[{"lang":"eng","text":"Lamellipodia are flat membrane protrusions formed during mesenchymal motion. Polymerization at the leading edge assembles the actin filament network and generates protrusion force. How this force is supported by the network and how the assembly rate is shared between protrusion and network retrograde flow determines the protrusion rate. We use mathematical modeling to understand experiments changing the F-actin density in lamellipodia of B16-F1 melanoma cells by modulation of Arp2/3 complex activity or knockout of the formins FMNL2 and FMNL3. Cells respond to a reduction of density with a decrease of protrusion velocity, an increase in the ratio of force to filament number, but constant network assembly rate. The relation between protrusion force and tension gradient in the F-actin network and the density dependency of friction, elasticity, and viscosity of the network explain the experimental observations. The formins act as filament nucleators and elongators with differential rates. Modulation of their activity suggests an effect on network assembly rate. Contrary to these expectations, the effect of changes in elongator composition is much weaker than the consequences of the density change. We conclude that the force acting on the leading edge membrane is the force required to drive F-actin network retrograde flow."}],"volume":29,"issue":"22","license":"https://creativecommons.org/licenses/by-nc-sa/4.0/","file":[{"relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_id":"5994","checksum":"e98465b4416b3e804c47f40086932af2","creator":"kschuh","file_size":6668971,"date_updated":"2020-07-14T12:47:15Z","file_name":"2018_ASCB_Dolati.pdf","date_created":"2019-02-14T12:34:29Z"}],"language":[{"iso":"eng"}],"publication_identifier":{"eissn":["1939-4586"]},"publication_status":"published"},{"oa_version":"Published Version","abstract":[{"text":"T cells are actively scanning pMHC-presenting cells in lymphoid organs and nonlymphoid tissues (NLTs) with divergent topologies and confinement. How the T cell actomyosin cytoskeleton facilitates this task in distinct environments is incompletely understood. Here, we show that lack of Myosin IXb (Myo9b), a negative regulator of the small GTPase Rho, led to increased Rho-GTP levels and cell surface stiffness in primary T cells. Nonetheless, intravital imaging revealed robust motility of Myo9b−/− CD8+ T cells in lymphoid tissue and similar expansion and differentiation during immune responses. In contrast, accumulation of Myo9b−/− CD8+ T cells in NLTs was strongly impaired. Specifically, Myo9b was required for T cell crossing of basement membranes, such as those which are present between dermis and epidermis. As consequence, Myo9b−/− CD8+ T cells showed impaired control of skin infections. In sum, we show that Myo9b is critical for the CD8+ T cell adaptation from lymphoid to NLT surveillance and the establishment of protective tissue–resident T cell populations.","lang":"eng"}],"intvolume":" 2015","month":"06","scopus_import":"1","language":[{"iso":"eng"}],"file":[{"checksum":"86ae5331f9bfced9a6358a790a04bef4","file_id":"6498","content_type":"application/pdf","access_level":"open_access","relation":"main_file","date_created":"2019-05-28T12:40:05Z","file_name":"2018_rupress_Moalli.pdf","date_updated":"2020-07-14T12:47:32Z","file_size":3841660,"creator":"kschuh"}],"publication_status":"published","publication_identifier":{"eissn":["1540-9538"],"issn":["0022-1007"]},"volume":2015,"issue":"7","_id":"6497","status":"public","tmp":{"name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","image":"/images/cc_by_nc_sa.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","short":"CC BY-NC-SA (4.0)"},"type":"journal_article","ddc":["570"],"date_updated":"2023-09-19T14:52:08Z","file_date_updated":"2020-07-14T12:47:32Z","department":[{"_id":"MiSi"}],"oa":1,"publisher":"Rockefeller University Press","quality_controlled":"1","publication":"The Journal of Experimental Medicine","day":"06","year":"2018","isi":1,"has_accepted_license":"1","date_created":"2019-05-28T12:36:47Z","date_published":"2018-06-06T00:00:00Z","doi":"10.1084/jem.20170896","page":"1869–1890","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"ista":"Moalli F, Ficht X, Germann P, Vladymyrov M, Stolp B, de Vries I, Lyck R, Balmer J, Fiocchi A, Kreutzfeldt M, Merkler D, Iannacone M, Ariga A, Stoffel MH, Sharpe J, Bähler M, Sixt MK, Diz-Muñoz A, Stein JV. 2018. The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. The Journal of Experimental Medicine. 2015(7), 1869–1890.","chicago":"Moalli, Federica, Xenia Ficht, Philipp Germann, Mykhailo Vladymyrov, Bettina Stolp, Ingrid de Vries, Ruth Lyck, et al. “The Rho Regulator Myosin IXb Enables Nonlymphoid Tissue Seeding of Protective CD8+T Cells.” The Journal of Experimental Medicine. Rockefeller University Press, 2018. https://doi.org/10.1084/jem.20170896.","ama":"Moalli F, Ficht X, Germann P, et al. The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. The Journal of Experimental Medicine. 2018;2015(7):1869–1890. doi:10.1084/jem.20170896","apa":"Moalli, F., Ficht, X., Germann, P., Vladymyrov, M., Stolp, B., de Vries, I., … Stein, J. V. (2018). The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. The Journal of Experimental Medicine. Rockefeller University Press. https://doi.org/10.1084/jem.20170896","ieee":"F. Moalli et al., “The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells,” The Journal of Experimental Medicine, vol. 2015, no. 7. Rockefeller University Press, pp. 1869–1890, 2018.","short":"F. Moalli, X. Ficht, P. Germann, M. Vladymyrov, B. Stolp, I. de Vries, R. Lyck, J. Balmer, A. Fiocchi, M. Kreutzfeldt, D. Merkler, M. Iannacone, A. Ariga, M.H. Stoffel, J. Sharpe, M. Bähler, M.K. Sixt, A. Diz-Muñoz, J.V. Stein, The Journal of Experimental Medicine 2015 (2018) 1869–1890.","mla":"Moalli, Federica, et al. “The Rho Regulator Myosin IXb Enables Nonlymphoid Tissue Seeding of Protective CD8+T Cells.” The Journal of Experimental Medicine, vol. 2015, no. 7, Rockefeller University Press, 2018, pp. 1869–1890, doi:10.1084/jem.20170896."},"title":"The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells","article_processing_charge":"No","external_id":{"isi":["000440822900011"]},"author":[{"last_name":"Moalli","full_name":"Moalli, Federica","first_name":"Federica"},{"first_name":"Xenia","last_name":"Ficht","full_name":"Ficht, Xenia"},{"last_name":"Germann","full_name":"Germann, Philipp","first_name":"Philipp"},{"full_name":"Vladymyrov, Mykhailo","last_name":"Vladymyrov","first_name":"Mykhailo"},{"full_name":"Stolp, Bettina","last_name":"Stolp","first_name":"Bettina"},{"first_name":"Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","full_name":"de Vries, Ingrid","last_name":"de Vries"},{"first_name":"Ruth","full_name":"Lyck, Ruth","last_name":"Lyck"},{"last_name":"Balmer","full_name":"Balmer, Jasmin","first_name":"Jasmin"},{"first_name":"Amleto","last_name":"Fiocchi","full_name":"Fiocchi, Amleto"},{"first_name":"Mario","last_name":"Kreutzfeldt","full_name":"Kreutzfeldt, Mario"},{"first_name":"Doron","last_name":"Merkler","full_name":"Merkler, Doron"},{"first_name":"Matteo","last_name":"Iannacone","full_name":"Iannacone, Matteo"},{"full_name":"Ariga, Akitaka","last_name":"Ariga","first_name":"Akitaka"},{"first_name":"Michael H.","full_name":"Stoffel, Michael H.","last_name":"Stoffel"},{"last_name":"Sharpe","full_name":"Sharpe, James","first_name":"James"},{"first_name":"Martin","full_name":"Bähler, Martin","last_name":"Bähler"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Alba","full_name":"Diz-Muñoz, Alba","last_name":"Diz-Muñoz"},{"first_name":"Jens V.","full_name":"Stein, Jens V.","last_name":"Stein"}]},{"status":"public","article_type":"original","type":"journal_article","_id":"402","department":[{"_id":"MiSi"}],"date_updated":"2024-03-27T23:30:09Z","month":"03","intvolume":" 359","scopus_import":"1","main_file_link":[{"url":"https://doi.org/10.1126/science.aal3662","open_access":"1"}],"pmid":1,"oa_version":"Published Version","acknowledged_ssus":[{"_id":"Bio"}],"abstract":[{"lang":"eng","text":"During metastasis, malignant cells escape the primary tumor, intravasate lymphatic vessels, and reach draining sentinel lymph nodes before they colonize distant organs via the blood circulation. Although lymph node metastasis in cancer patients correlates with poor prognosis, evidence is lacking as to whether and how tumor cells enter the bloodstream via lymph nodes. To investigate this question, we delivered carcinoma cells into the lymph nodes of mice by microinfusing the cells into afferent lymphatic vessels. We found that tumor cells rapidly infiltrated the lymph node parenchyma, invaded blood vessels, and seeded lung metastases without involvement of the thoracic duct. These results suggest that the lymph node blood vessels can serve as an exit route for systemic dissemination of cancer cells in experimental mouse models. Whether this form of tumor cell spreading occurs in cancer patients remains to be determined."}],"volume":359,"issue":"6382","related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"6947"}]},"ec_funded":1,"language":[{"iso":"eng"}],"publication_status":"published","project":[{"call_identifier":"FWF","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","grant_number":"Y 564-B12","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)"},{"call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","grant_number":"281556","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)"}],"title":"Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice","publist_id":"7428","author":[{"full_name":"Brown, Markus","last_name":"Brown","first_name":"Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0003-3470-6119","full_name":"Assen, Frank P","last_name":"Assen","first_name":"Frank P","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","full_name":"Leithner, Alexander F","orcid":"0000-0002-1073-744X","last_name":"Leithner"},{"first_name":"Jun","last_name":"Abe","full_name":"Abe, Jun"},{"first_name":"Helga","full_name":"Schachner, Helga","last_name":"Schachner"},{"first_name":"Gabriele","last_name":"Asfour","full_name":"Asfour, Gabriele"},{"first_name":"Zsuzsanna","last_name":"Bagó Horváth","full_name":"Bagó Horváth, Zsuzsanna"},{"first_name":"Jens","full_name":"Stein, Jens","last_name":"Stein"},{"first_name":"Pavel","last_name":"Uhrin","full_name":"Uhrin, Pavel"},{"last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Kerjaschki","full_name":"Kerjaschki, Dontscho","first_name":"Dontscho"}],"external_id":{"isi":["000428043600047"],"pmid":["29567714"]},"article_processing_charge":"No","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"ista":"Brown M, Assen FP, Leithner AF, Abe J, Schachner H, Asfour G, Bagó Horváth Z, Stein J, Uhrin P, Sixt MK, Kerjaschki D. 2018. Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. Science. 359(6382), 1408–1411.","chicago":"Brown, Markus, Frank P Assen, Alexander F Leithner, Jun Abe, Helga Schachner, Gabriele Asfour, Zsuzsanna Bagó Horváth, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” Science. American Association for the Advancement of Science, 2018. https://doi.org/10.1126/science.aal3662.","apa":"Brown, M., Assen, F. P., Leithner, A. F., Abe, J., Schachner, H., Asfour, G., … Kerjaschki, D. (2018). Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.aal3662","ama":"Brown M, Assen FP, Leithner AF, et al. Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. Science. 2018;359(6382):1408-1411. doi:10.1126/science.aal3662","short":"M. Brown, F.P. Assen, A.F. Leithner, J. Abe, H. Schachner, G. Asfour, Z. Bagó Horváth, J. Stein, P. Uhrin, M.K. Sixt, D. Kerjaschki, Science 359 (2018) 1408–1411.","ieee":"M. Brown et al., “Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice,” Science, vol. 359, no. 6382. American Association for the Advancement of Science, pp. 1408–1411, 2018.","mla":"Brown, Markus, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” Science, vol. 359, no. 6382, American Association for the Advancement of Science, 2018, pp. 1408–11, doi:10.1126/science.aal3662."},"publisher":"American Association for the Advancement of Science","quality_controlled":"1","oa":1,"acknowledgement":"M.B. was supported by the Cell Communication in Health and Disease graduate study program of the Austrian Science Fund (FWF) and the Medical University of Vienna. M.S. was supported by the European Research Council (grant ERC GA 281556) and an FWF START award.\r\nWe thank C. Moussion for establishing the intralymphatic injection at IST Austria and for providing anti-PNAd hybridoma supernatant, R. Förster and A. Braun for sharing the intralymphatic injection technology, K. Vaahtomeri for the lentiviral constructs, M. Hons for establishing in vivo multiphoton imaging, the Sixt lab for intellectual input, M. Schunn for help with the design of the in vivo experiments, F. Langer for technical assistance with the in vivo experiments, the bioimaging facility of IST Austria for support, and R. Efferl for providing the CT26 cell line.","date_published":"2018-03-23T00:00:00Z","doi":"10.1126/science.aal3662","date_created":"2018-12-11T11:46:16Z","page":"1408 - 1411","day":"23","publication":"Science","isi":1,"year":"2018"},{"department":[{"_id":"MiSi"}],"file_date_updated":"2021-02-11T23:30:17Z","ddc":["571","599","610"],"date_updated":"2023-09-07T12:39:44Z","supervisor":[{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"pubrep_id":"998","status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"dissertation","_id":"323","related_material":{"record":[{"status":"public","id":"1321","relation":"part_of_dissertation"}]},"language":[{"iso":"eng"}],"file":[{"date_created":"2019-04-05T09:23:11Z","file_name":"PhD_thesis_AlexLeithner_final_version.docx","creator":"dernst","date_updated":"2021-02-11T23:30:17Z","file_size":29027671,"file_id":"6219","checksum":"d5e3edbac548c26c1fa43a4b37a54a4c","access_level":"closed","relation":"source_file","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","embargo_to":"open_access"},{"relation":"main_file","access_level":"open_access","content_type":"application/pdf","embargo":"2019-04-15","file_id":"6220","checksum":"071f7476db29e41146824ebd0697cb10","creator":"dernst","file_size":66045341,"date_updated":"2021-02-11T11:17:16Z","file_name":"PhD_thesis_AlexLeithner.pdf","date_created":"2019-04-05T09:23:11Z"}],"degree_awarded":"PhD","publication_status":"published","publication_identifier":{"issn":["2663-337X"]},"month":"04","alternative_title":["ISTA Thesis"],"oa_version":"Published Version","acknowledged_ssus":[{"_id":"NanoFab"},{"_id":"Bio"},{"_id":"PreCl"},{"_id":"EM-Fac"}],"abstract":[{"text":"In the here presented thesis, we explore the role of branched actin networks in cell migration and antigen presentation, the two most relevant processes in dendritic cell biology. Branched actin networks construct lamellipodial protrusions at the leading edge of migrating cells. These are typically seen as adhesive structures, which mediate force transduction to the extracellular matrix that leads to forward locomotion. We ablated Arp2/3 nucleation promoting factor WAVE in DCs and found that the resulting cells lack lamellipodial protrusions. Instead, depending on the maturation state, one or multiple filopodia were formed. By challenging these cells in a variety of migration assays we found that lamellipodial protrusions are dispensable for the locomotion of leukocytes and actually dampen the speed of migration. However, lamellipodia are critically required to negotiate complex environments that DCs experience while they travel to the next draining lymph node. Taken together our results suggest that leukocyte lamellipodia have rather a sensory- than a force transducing function. Furthermore, we show for the first time structure and dynamics of dendritic cell F-actin at the immunological synapse with naïve T cells. Dendritic cell F-actin appears as dynamic foci that are nucleated by the Arp2/3 complex. WAVE ablated dendritic cells show increased membrane tension, leading to an altered ultrastructure of the immunological synapse and severe T cell priming defects. These results point towards a previously unappreciated role of the cellular mechanics of dendritic cells in T cell activation. Additionally, we present a novel cell culture based system for the differentiation of dendritic cells from conditionally immortalized hematopoietic precursors. These precursor cells are genetically tractable via the CRISPR/Cas9 system while they retain their ability to differentiate into highly migratory dendritic cells and other immune cells. This will foster the study of all aspects of dendritic cell biology and beyond. ","lang":"eng"}],"title":"Branched actin networks in dendritic cell biology","article_processing_charge":"No","publist_id":"7542","author":[{"first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","full_name":"Leithner, Alexander F","orcid":"0000-0002-1073-744X","last_name":"Leithner"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"chicago":"Leithner, Alexander F. “Branched Actin Networks in Dendritic Cell Biology.” Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th_998.","ista":"Leithner AF. 2018. Branched actin networks in dendritic cell biology. Institute of Science and Technology Austria.","mla":"Leithner, Alexander F. Branched Actin Networks in Dendritic Cell Biology. Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th_998.","apa":"Leithner, A. F. (2018). Branched actin networks in dendritic cell biology. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_998","ama":"Leithner AF. Branched actin networks in dendritic cell biology. 2018. doi:10.15479/AT:ISTA:th_998","ieee":"A. F. Leithner, “Branched actin networks in dendritic cell biology,” Institute of Science and Technology Austria, 2018.","short":"A.F. Leithner, Branched Actin Networks in Dendritic Cell Biology, Institute of Science and Technology Austria, 2018."},"date_created":"2018-12-11T11:45:49Z","date_published":"2018-04-12T00:00:00Z","doi":"10.15479/AT:ISTA:th_998","page":"99","day":"12","year":"2018","has_accepted_license":"1","oa":1,"publisher":"Institute of Science and Technology Austria","acknowledgement":"First of all I would like to thank Michael Sixt for giving me the opportunity to work in \r\nhis group and for his support throughout the years. He is a truly inspiring person and \r\nthe best boss one can imagine. I would also like to thank all current and past \r\nmembers of the Sixt group for their help and the great working atmosphere in the lab. \r\nIt is a true privilege to work with such a bright, funny and friendly group of people and \r\nI’m proud that I could be part of it. Furthermore, I would like to say ‘thank you’ to Daria Siekhaus for all the meetings and discussion we had throughout the years \r\nand to Federica Benvenuti for being part of my committee. I am also grateful to Jack \r\nMerrin in the nanofabrication facility and all the people working in the bioimaging-\r\n, the electron microscopy- and the preclinical facilities."},{"_id":"15","status":"public","type":"journal_article","date_updated":"2024-03-27T23:30:39Z","department":[{"_id":"MiSi"},{"_id":"Bio"}],"oa_version":"Published Version","pmid":1,"abstract":[{"lang":"eng","text":"Although much is known about the physiological framework of T cell motility, and numerous rate-limiting molecules have been identified through loss-of-function approaches, an integrated functional concept of T cell motility is lacking. Here, we used in vivo precision morphometry together with analysis of cytoskeletal dynamics in vitro to deconstruct the basic mechanisms of T cell migration within lymphatic organs. We show that the contributions of the integrin LFA-1 and the chemokine receptor CCR7 are complementary rather than positioned in a linear pathway, as they are during leukocyte extravasation from the blood vasculature. Our data demonstrate that CCR7 controls cortical actin flows, whereas integrins mediate substrate friction that is sufficient to drive locomotion in the absence of considerable surface adhesions and plasma membrane flux."}],"acknowledged_ssus":[{"_id":"SSU"}],"intvolume":" 19","month":"05","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pubmed/29777221","open_access":"1"}],"scopus_import":"1","language":[{"iso":"eng"}],"publication_status":"published","ec_funded":1,"volume":19,"issue":"6","related_material":{"record":[{"id":"6891","status":"public","relation":"dissertation_contains"}]},"project":[{"call_identifier":"H2020","_id":"25FE9508-B435-11E9-9278-68D0E5697425","name":"Cellular navigation along spatial gradients","grant_number":"724373"},{"grant_number":"747687","name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells","call_identifier":"H2020","_id":"260AA4E2-B435-11E9-9278-68D0E5697425"},{"grant_number":"ALTF 1396-2014","name":"Molecular and system level view of immune cell migration","_id":"25A48D24-B435-11E9-9278-68D0E5697425"},{"call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","grant_number":"281556","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"mla":"Hons, Miroslav, et al. “Chemokines and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal Migration of T Cells.” Nature Immunology, vol. 19, no. 6, Nature Publishing Group, 2018, pp. 606–16, doi:10.1038/s41590-018-0109-z.","ieee":"M. Hons et al., “Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells,” Nature Immunology, vol. 19, no. 6. Nature Publishing Group, pp. 606–616, 2018.","short":"M. Hons, A. Kopf, R. Hauschild, A.F. Leithner, F.R. Gärtner, J. Abe, J. Renkawitz, J. Stein, M.K. Sixt, Nature Immunology 19 (2018) 606–616.","apa":"Hons, M., Kopf, A., Hauschild, R., Leithner, A. F., Gärtner, F. R., Abe, J., … Sixt, M. K. (2018). Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/s41590-018-0109-z","ama":"Hons M, Kopf A, Hauschild R, et al. Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. Nature Immunology. 2018;19(6):606-616. doi:10.1038/s41590-018-0109-z","chicago":"Hons, Miroslav, Aglaja Kopf, Robert Hauschild, Alexander F Leithner, Florian R Gärtner, Jun Abe, Jörg Renkawitz, Jens Stein, and Michael K Sixt. “Chemokines and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal Migration of T Cells.” Nature Immunology. Nature Publishing Group, 2018. https://doi.org/10.1038/s41590-018-0109-z.","ista":"Hons M, Kopf A, Hauschild R, Leithner AF, Gärtner FR, Abe J, Renkawitz J, Stein J, Sixt MK. 2018. Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. Nature Immunology. 19(6), 606–616."},"title":"Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells","external_id":{"pmid":["29777221"],"isi":["000433041500026"]},"article_processing_charge":"No","publist_id":"8040","author":[{"last_name":"Hons","full_name":"Hons, Miroslav","orcid":"0000-0002-6625-3348","id":"4167FE56-F248-11E8-B48F-1D18A9856A87","first_name":"Miroslav"},{"id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87","first_name":"Aglaja","last_name":"Kopf","orcid":"0000-0002-2187-6656","full_name":"Kopf, Aglaja"},{"first_name":"Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","last_name":"Hauschild","orcid":"0000-0001-9843-3522","full_name":"Hauschild, Robert"},{"last_name":"Leithner","full_name":"Leithner, Alexander F","orcid":"0000-0002-1073-744X","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander F"},{"first_name":"Florian R","id":"397A88EE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6120-3723","full_name":"Gärtner, Florian R","last_name":"Gärtner"},{"first_name":"Jun","full_name":"Abe, Jun","last_name":"Abe"},{"first_name":"Jörg","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2856-3369","full_name":"Renkawitz, Jörg","last_name":"Renkawitz"},{"first_name":"Jens","full_name":"Stein, Jens","last_name":"Stein"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt"}],"acknowledgement":"This work was funded by grants from the European Research Council (ERC StG 281556 and CoG 724373) and the Austrian Science Foundation (FWF) to M.S. and by Swiss National Foundation (SNF) project grants 31003A_135649, 31003A_153457 and CR23I3_156234 to J.V.S. F.G. received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 747687, and J.R. was funded by an EMBO long-term fellowship (ALTF 1396-2014).","oa":1,"quality_controlled":"1","publisher":"Nature Publishing Group","publication":"Nature Immunology","day":"18","year":"2018","isi":1,"date_created":"2018-12-11T11:44:10Z","date_published":"2018-05-18T00:00:00Z","doi":"10.1038/s41590-018-0109-z","page":"606 - 616"},{"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","pubrep_id":"919","status":"public","_id":"569","file_date_updated":"2020-07-14T12:47:10Z","department":[{"_id":"MiSi"}],"date_updated":"2023-02-23T12:30:29Z","ddc":["570"],"scopus_import":1,"intvolume":" 6","month":"11","abstract":[{"lang":"eng","text":"The actomyosin ring generates force to ingress the cytokinetic cleavage furrow in animal cells, yet its filament organization and the mechanism of contractility is not well understood. We quantified actin filament order in human cells using fluorescence polarization microscopy and found that cleavage furrow ingression initiates by contraction of an equatorial actin network with randomly oriented filaments. The network subsequently gradually reoriented actin filaments along the cell equator. This strictly depended on myosin II activity, suggesting local network reorganization by mechanical forces. Cortical laser microsurgery revealed that during cytokinesis progression, mechanical tension increased substantially along the direction of the cell equator, while the network contracted laterally along the pole-to-pole axis without a detectable increase in tension. Our data suggest that an asymmetric increase in cortical tension promotes filament reorientation along the cytokinetic cleavage furrow, which might have implications for diverse other biological processes involving actomyosin rings."}],"oa_version":"Published Version","volume":6,"publication_status":"published","publication_identifier":{"issn":["2050084X"]},"language":[{"iso":"eng"}],"file":[{"date_updated":"2020-07-14T12:47:10Z","file_size":9666973,"creator":"system","date_created":"2018-12-12T10:10:40Z","file_name":"IST-2017-919-v1+1_elife-30867-figures-v1.pdf","content_type":"application/pdf","access_level":"open_access","relation":"main_file","file_id":"4829","checksum":"ba09c1451153d39e4f4b7cee013e314c"},{"file_name":"IST-2017-919-v1+2_elife-30867-v1.pdf","date_created":"2018-12-12T10:10:41Z","creator":"system","file_size":5951246,"date_updated":"2020-07-14T12:47:10Z","file_id":"4830","checksum":"01eb51f1d6ad679947415a51c988e137","relation":"main_file","access_level":"open_access","content_type":"application/pdf"}],"article_number":"e30867","author":[{"last_name":"Spira","full_name":"Spira, Felix","first_name":"Felix"},{"first_name":"Sara","full_name":"Cuylen Haering, Sara","last_name":"Cuylen Haering"},{"last_name":"Mehta","full_name":"Mehta, Shalin","first_name":"Shalin"},{"first_name":"Matthias","full_name":"Samwer, Matthias","last_name":"Samwer"},{"id":"35B76592-F248-11E8-B48F-1D18A9856A87","first_name":"Anne","full_name":"Reversat, Anne","orcid":"0000-0003-0666-8928","last_name":"Reversat"},{"full_name":"Verma, Amitabh","last_name":"Verma","first_name":"Amitabh"},{"first_name":"Rudolf","last_name":"Oldenbourg","full_name":"Oldenbourg, Rudolf"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"},{"first_name":"Daniel","last_name":"Gerlich","full_name":"Gerlich, Daniel"}],"publist_id":"7245","title":"Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments","citation":{"mla":"Spira, Felix, et al. “Cytokinesis in Vertebrate Cells Initiates by Contraction of an Equatorial Actomyosin Network Composed of Randomly Oriented Filaments.” ELife, vol. 6, e30867, eLife Sciences Publications, 2017, doi:10.7554/eLife.30867.","short":"F. Spira, S. Cuylen Haering, S. Mehta, M. Samwer, A. Reversat, A. Verma, R. Oldenbourg, M.K. Sixt, D. Gerlich, ELife 6 (2017).","ieee":"F. Spira et al., “Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments,” eLife, vol. 6. eLife Sciences Publications, 2017.","ama":"Spira F, Cuylen Haering S, Mehta S, et al. Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. eLife. 2017;6. doi:10.7554/eLife.30867","apa":"Spira, F., Cuylen Haering, S., Mehta, S., Samwer, M., Reversat, A., Verma, A., … Gerlich, D. (2017). Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.30867","chicago":"Spira, Felix, Sara Cuylen Haering, Shalin Mehta, Matthias Samwer, Anne Reversat, Amitabh Verma, Rudolf Oldenbourg, Michael K Sixt, and Daniel Gerlich. “Cytokinesis in Vertebrate Cells Initiates by Contraction of an Equatorial Actomyosin Network Composed of Randomly Oriented Filaments.” ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.30867.","ista":"Spira F, Cuylen Haering S, Mehta S, Samwer M, Reversat A, Verma A, Oldenbourg R, Sixt MK, Gerlich D. 2017. Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. eLife. 6, e30867."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","oa":1,"quality_controlled":"1","publisher":"eLife Sciences Publications","date_created":"2018-12-11T11:47:14Z","date_published":"2017-11-06T00:00:00Z","doi":"10.7554/eLife.30867","year":"2017","has_accepted_license":"1","publication":"eLife","day":"06"},{"page":"1368 - 1382","date_created":"2018-12-11T11:47:15Z","date_published":"2017-11-30T00:00:00Z","doi":"10.1016/j.cell.2017.11.001","year":"2017","publication":"Cell Press","day":"30","quality_controlled":"1","publisher":"Cell Press","author":[{"full_name":"Gärtner, Florian R","orcid":"0000-0001-6120-3723","last_name":"Gärtner","id":"397A88EE-F248-11E8-B48F-1D18A9856A87","first_name":"Florian R"},{"first_name":"Zerkah","last_name":"Ahmad","full_name":"Ahmad, Zerkah"},{"last_name":"Rosenberger","full_name":"Rosenberger, Gerhild","first_name":"Gerhild"},{"first_name":"Shuxia","last_name":"Fan","full_name":"Fan, Shuxia"},{"full_name":"Nicolai, Leo","last_name":"Nicolai","first_name":"Leo"},{"full_name":"Busch, Benjamin","last_name":"Busch","first_name":"Benjamin"},{"first_name":"Gökce","last_name":"Yavuz","full_name":"Yavuz, Gökce"},{"first_name":"Manja","full_name":"Luckner, Manja","last_name":"Luckner"},{"last_name":"Ishikawa Ankerhold","full_name":"Ishikawa Ankerhold, Hellen","first_name":"Hellen"},{"first_name":"Roman","full_name":"Hennel, Roman","last_name":"Hennel"},{"full_name":"Benechet, Alexandre","last_name":"Benechet","first_name":"Alexandre"},{"first_name":"Michael","full_name":"Lorenz, Michael","last_name":"Lorenz"},{"last_name":"Chandraratne","full_name":"Chandraratne, Sue","first_name":"Sue"},{"full_name":"Schubert, Irene","last_name":"Schubert","first_name":"Irene"},{"last_name":"Helmer","full_name":"Helmer, Sebastian","first_name":"Sebastian"},{"first_name":"Bianca","full_name":"Striednig, Bianca","last_name":"Striednig"},{"last_name":"Stark","full_name":"Stark, Konstantin","first_name":"Konstantin"},{"last_name":"Janko","full_name":"Janko, Marek","first_name":"Marek"},{"full_name":"Böttcher, Ralph","last_name":"Böttcher","first_name":"Ralph"},{"first_name":"Admar","full_name":"Verschoor, Admar","last_name":"Verschoor"},{"last_name":"Leon","full_name":"Leon, Catherine","first_name":"Catherine"},{"full_name":"Gachet, Christian","last_name":"Gachet","first_name":"Christian"},{"first_name":"Thomas","full_name":"Gudermann, Thomas","last_name":"Gudermann"},{"full_name":"Mederos Y Schnitzler, Michael","last_name":"Mederos Y Schnitzler","first_name":"Michael"},{"last_name":"Pincus","full_name":"Pincus, Zachary","first_name":"Zachary"},{"full_name":"Iannacone, Matteo","last_name":"Iannacone","first_name":"Matteo"},{"full_name":"Haas, Rainer","last_name":"Haas","first_name":"Rainer"},{"first_name":"Gerhard","last_name":"Wanner","full_name":"Wanner, Gerhard"},{"last_name":"Lauber","full_name":"Lauber, Kirsten","first_name":"Kirsten"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179"},{"first_name":"Steffen","last_name":"Massberg","full_name":"Massberg, Steffen"}],"publist_id":"7243","title":"Migrating platelets are mechano scavengers that collect and bundle bacteria","citation":{"mla":"Gärtner, Florian R., et al. “Migrating Platelets Are Mechano Scavengers That Collect and Bundle Bacteria.” Cell Press, vol. 171, no. 6, Cell Press, 2017, pp. 1368–82, doi:10.1016/j.cell.2017.11.001.","short":"F.R. Gärtner, Z. Ahmad, G. Rosenberger, S. Fan, L. Nicolai, B. Busch, G. Yavuz, M. Luckner, H. Ishikawa Ankerhold, R. Hennel, A. Benechet, M. Lorenz, S. Chandraratne, I. Schubert, S. Helmer, B. Striednig, K. Stark, M. Janko, R. Böttcher, A. Verschoor, C. Leon, C. Gachet, T. Gudermann, M. Mederos Y Schnitzler, Z. Pincus, M. Iannacone, R. Haas, G. Wanner, K. Lauber, M.K. Sixt, S. Massberg, Cell Press 171 (2017) 1368–1382.","ieee":"F. R. Gärtner et al., “Migrating platelets are mechano scavengers that collect and bundle bacteria,” Cell Press, vol. 171, no. 6. Cell Press, pp. 1368–1382, 2017.","apa":"Gärtner, F. R., Ahmad, Z., Rosenberger, G., Fan, S., Nicolai, L., Busch, B., … Massberg, S. (2017). Migrating platelets are mechano scavengers that collect and bundle bacteria. Cell Press. Cell Press. https://doi.org/10.1016/j.cell.2017.11.001","ama":"Gärtner FR, Ahmad Z, Rosenberger G, et al. Migrating platelets are mechano scavengers that collect and bundle bacteria. Cell Press. 2017;171(6):1368-1382. doi:10.1016/j.cell.2017.11.001","chicago":"Gärtner, Florian R, Zerkah Ahmad, Gerhild Rosenberger, Shuxia Fan, Leo Nicolai, Benjamin Busch, Gökce Yavuz, et al. “Migrating Platelets Are Mechano Scavengers That Collect and Bundle Bacteria.” Cell Press. Cell Press, 2017. https://doi.org/10.1016/j.cell.2017.11.001.","ista":"Gärtner FR, Ahmad Z, Rosenberger G, Fan S, Nicolai L, Busch B, Yavuz G, Luckner M, Ishikawa Ankerhold H, Hennel R, Benechet A, Lorenz M, Chandraratne S, Schubert I, Helmer S, Striednig B, Stark K, Janko M, Böttcher R, Verschoor A, Leon C, Gachet C, Gudermann T, Mederos Y Schnitzler M, Pincus Z, Iannacone M, Haas R, Wanner G, Lauber K, Sixt MK, Massberg S. 2017. Migrating platelets are mechano scavengers that collect and bundle bacteria. Cell Press. 171(6), 1368–1382."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","project":[{"name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells","grant_number":"747687","call_identifier":"H2020","_id":"260AA4E2-B435-11E9-9278-68D0E5697425"}],"ec_funded":1,"issue":"6","volume":171,"publication_status":"published","publication_identifier":{"issn":["00928674"]},"language":[{"iso":"eng"}],"scopus_import":1,"intvolume":" 171","month":"11","abstract":[{"text":"Blood platelets are critical for hemostasis and thrombosis and play diverse roles during immune responses. Despite these versatile tasks in mammalian biology, their skills on a cellular level are deemed limited, mainly consisting in rolling, adhesion, and aggregate formation. Here, we identify an unappreciated asset of platelets and show that adherent platelets use adhesion receptors to mechanically probe the adhesive substrate in their local microenvironment. When actomyosin-dependent traction forces overcome substrate resistance, platelets migrate and pile up the adhesive substrate together with any bound particulate material. They use this ability to act as cellular scavengers, scanning the vascular surface for potential invaders and collecting deposited bacteria. Microbe collection by migrating platelets boosts the activity of professional phagocytes, exacerbating inflammatory tissue injury in sepsis. This assigns platelets a central role in innate immune responses and identifies them as potential targets to dampen inflammatory tissue damage in clinical scenarios of severe systemic infection. In addition to their role in thrombosis and hemostasis, platelets can also migrate to sites of infection to help trap bacteria and clear the vascular surface.","lang":"eng"}],"oa_version":"None","department":[{"_id":"MiSi"}],"date_updated":"2021-01-12T08:03:15Z","type":"journal_article","status":"public","_id":"571"},{"volume":8,"publication_status":"published","publication_identifier":{"issn":["20411723"]},"language":[{"iso":"eng"}],"file":[{"file_id":"5072","checksum":"dae30190291c3630e8102d8714a8d23e","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"IST-2017-902-v1+1_Kage_et_al-2017-Nature_Communications.pdf","date_created":"2018-12-12T10:14:21Z","creator":"system","file_size":9523746,"date_updated":"2020-07-14T12:47:34Z"}],"scopus_import":1,"intvolume":" 8","month":"03","abstract":[{"lang":"eng","text":"Migration frequently involves Rac-mediated protrusion of lamellipodia, formed by Arp2/3 complex-dependent branching thought to be crucial for force generation and stability of these networks. The formins FMNL2 and FMNL3 are Cdc42 effectors targeting to the lamellipodium tip and shown here to nucleate and elongate actin filaments with complementary activities in vitro. In migrating B16-F1 melanoma cells, both formins contribute to the velocity of lamellipodium protrusion. Loss of FMNL2/3 function in melanoma cells and fibroblasts reduces lamellipodial width, actin filament density and -bundling, without changing patterns of Arp2/3 complex incorporation. Strikingly, in melanoma cells, FMNL2/3 gene inactivation almost completely abolishes protrusion forces exerted by lamellipodia and modifies their ultrastructural organization. Consistently, CRISPR/Cas-mediated depletion of FMNL2/3 in fibroblasts reduces both migration and capability of cells to move against viscous media. Together, we conclude that force generation in lamellipodia strongly depends on FMNL formin activity, operating in addition to Arp2/3 complex-dependent filament branching."}],"oa_version":"Published Version","file_date_updated":"2020-07-14T12:47:34Z","department":[{"_id":"MiSi"}],"date_updated":"2021-01-12T08:08:06Z","ddc":["570"],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","pubrep_id":"902","status":"public","_id":"659","date_created":"2018-12-11T11:47:46Z","doi":"10.1038/ncomms14832","date_published":"2017-03-22T00:00:00Z","year":"2017","has_accepted_license":"1","publication":"Nature Communications","day":"22","oa":1,"quality_controlled":"1","publisher":"Nature Publishing Group","article_processing_charge":"No","author":[{"first_name":"Frieda","last_name":"Kage","full_name":"Kage, Frieda"},{"full_name":"Winterhoff, Moritz","last_name":"Winterhoff","first_name":"Moritz"},{"first_name":"Vanessa","last_name":"Dimchev","full_name":"Dimchev, Vanessa"},{"last_name":"Müller","full_name":"Müller, Jan","first_name":"Jan","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D"},{"full_name":"Thalheim, Tobias","last_name":"Thalheim","first_name":"Tobias"},{"first_name":"Anika","last_name":"Freise","full_name":"Freise, Anika"},{"full_name":"Brühmann, Stefan","last_name":"Brühmann","first_name":"Stefan"},{"first_name":"Jana","full_name":"Kollasser, Jana","last_name":"Kollasser"},{"first_name":"Jennifer","full_name":"Block, Jennifer","last_name":"Block"},{"full_name":"Dimchev, Georgi A","last_name":"Dimchev","first_name":"Georgi A"},{"first_name":"Matthias","last_name":"Geyer","full_name":"Geyer, Matthias"},{"full_name":"Schnittler, Hams","last_name":"Schnittler","first_name":"Hams"},{"first_name":"Cord","full_name":"Brakebusch, Cord","last_name":"Brakebusch"},{"first_name":"Theresia","last_name":"Stradal","full_name":"Stradal, Theresia"},{"last_name":"Carlier","full_name":"Carlier, Marie","first_name":"Marie"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt"},{"first_name":"Josef","full_name":"Käs, Josef","last_name":"Käs"},{"first_name":"Jan","last_name":"Faix","full_name":"Faix, Jan"},{"first_name":"Klemens","last_name":"Rottner","full_name":"Rottner, Klemens"}],"publist_id":"7075","title":"FMNL formins boost lamellipodial force generation","citation":{"apa":"Kage, F., Winterhoff, M., Dimchev, V., Müller, J., Thalheim, T., Freise, A., … Rottner, K. (2017). FMNL formins boost lamellipodial force generation. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms14832","ama":"Kage F, Winterhoff M, Dimchev V, et al. FMNL formins boost lamellipodial force generation. Nature Communications. 2017;8. doi:10.1038/ncomms14832","short":"F. Kage, M. Winterhoff, V. Dimchev, J. Müller, T. Thalheim, A. Freise, S. Brühmann, J. Kollasser, J. Block, G.A. Dimchev, M. Geyer, H. Schnittler, C. Brakebusch, T. Stradal, M. Carlier, M.K. Sixt, J. Käs, J. Faix, K. Rottner, Nature Communications 8 (2017).","ieee":"F. Kage et al., “FMNL formins boost lamellipodial force generation,” Nature Communications, vol. 8. Nature Publishing Group, 2017.","mla":"Kage, Frieda, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature Communications, vol. 8, 14832, Nature Publishing Group, 2017, doi:10.1038/ncomms14832.","ista":"Kage F, Winterhoff M, Dimchev V, Müller J, Thalheim T, Freise A, Brühmann S, Kollasser J, Block J, Dimchev GA, Geyer M, Schnittler H, Brakebusch C, Stradal T, Carlier M, Sixt MK, Käs J, Faix J, Rottner K. 2017. FMNL formins boost lamellipodial force generation. Nature Communications. 8, 14832.","chicago":"Kage, Frieda, Moritz Winterhoff, Vanessa Dimchev, Jan Müller, Tobias Thalheim, Anika Freise, Stefan Brühmann, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/ncomms14832."},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","article_number":"14832"},{"department":[{"_id":"MiSi"}],"file_date_updated":"2020-07-14T12:47:37Z","ddc":["570"],"date_updated":"2021-01-12T08:08:34Z","status":"public","article_type":"original","type":"journal_article","_id":"668","issue":"17","volume":292,"file":[{"creator":"dernst","file_size":5647880,"date_updated":"2020-07-14T12:47:37Z","file_name":"2017_JBC_Horsthemke.pdf","date_created":"2019-10-24T15:25:42Z","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_id":"6971","checksum":"d488162874326a4bb056065fa549dc4a"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["00219258"]},"publication_status":"published","month":"04","intvolume":" 292","scopus_import":1,"oa_version":"Published Version","abstract":[{"text":"Macrophage filopodia, finger-like membrane protrusions, were first implicated in phagocytosis more than 100 years ago, but little is still known about the involvement of these actin-dependent structures in particle clearance. Using spinning disk confocal microscopy to image filopodial dynamics in mouse resident Lifeact-EGFP macrophages, we show that filopodia, or filopodia-like structures, support pathogen clearance by multiple means. Filopodia supported the phagocytic uptake of bacterial (Escherichia coli) particles by (i) capturing along the filopodial shaft and surfing toward the cell body, the most common mode of capture; (ii) capturing via the tip followed by retraction; (iii) combinations of surfing and retraction; or (iv) sweeping actions. In addition, filopodia supported the uptake of zymosan (Saccharomyces cerevisiae) particles by (i) providing fixation, (ii) capturing at the tip and filopodia-guided actin anterograde flow with phagocytic cup formation, and (iii) the rapid growth of new protrusions. To explore the role of filopodia-inducing Cdc42, we generated myeloid-restricted Cdc42 knock-out mice. Cdc42-deficient macrophages exhibited rapid phagocytic cup kinetics, but reduced particle clearance, which could be explained by the marked rounded-up morphology of these cells. Macrophages lacking Myo10, thought to act downstream of Cdc42, had normal morphology, motility, and phagocytic cup formation, but displayed markedly reduced filopodia formation. In conclusion, live-cell imaging revealed multiple mechanisms involving macrophage filopodia in particle capture and engulfment. Cdc42 is not critical for filopodia or phagocytic cup formation, but plays a key role in driving macrophage lamellipodial spreading.","lang":"eng"}],"title":"Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion","publist_id":"7059","author":[{"first_name":"Markus","full_name":"Horsthemke, Markus","last_name":"Horsthemke"},{"full_name":"Bachg, Anne","last_name":"Bachg","first_name":"Anne"},{"full_name":"Groll, Katharina","last_name":"Groll","first_name":"Katharina"},{"last_name":"Moyzio","full_name":"Moyzio, Sven","first_name":"Sven"},{"last_name":"Müther","full_name":"Müther, Barbara","first_name":"Barbara"},{"first_name":"Sandra","last_name":"Hemkemeyer","full_name":"Hemkemeyer, Sandra"},{"first_name":"Roland","full_name":"Wedlich Söldner, Roland","last_name":"Wedlich Söldner"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"},{"last_name":"Tacke","full_name":"Tacke, Sebastian","first_name":"Sebastian"},{"last_name":"Bähler","full_name":"Bähler, Martin","first_name":"Martin"},{"first_name":"Peter","full_name":"Hanley, Peter","last_name":"Hanley"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"ista":"Horsthemke M, Bachg A, Groll K, Moyzio S, Müther B, Hemkemeyer S, Wedlich Söldner R, Sixt MK, Tacke S, Bähler M, Hanley P. 2017. Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. 292(17), 7258–7273.","chicago":"Horsthemke, Markus, Anne Bachg, Katharina Groll, Sven Moyzio, Barbara Müther, Sandra Hemkemeyer, Roland Wedlich Söldner, et al. “Multiple Roles of Filopodial Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal of Biological Chemistry. American Society for Biochemistry and Molecular Biology, 2017. https://doi.org/10.1074/jbc.M116.766923.","ieee":"M. Horsthemke et al., “Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion,” Journal of Biological Chemistry, vol. 292, no. 17. American Society for Biochemistry and Molecular Biology, pp. 7258–7273, 2017.","short":"M. Horsthemke, A. Bachg, K. Groll, S. Moyzio, B. Müther, S. Hemkemeyer, R. Wedlich Söldner, M.K. Sixt, S. Tacke, M. Bähler, P. Hanley, Journal of Biological Chemistry 292 (2017) 7258–7273.","apa":"Horsthemke, M., Bachg, A., Groll, K., Moyzio, S., Müther, B., Hemkemeyer, S., … Hanley, P. (2017). Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. American Society for Biochemistry and Molecular Biology. https://doi.org/10.1074/jbc.M116.766923","ama":"Horsthemke M, Bachg A, Groll K, et al. Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. 2017;292(17):7258-7273. doi:10.1074/jbc.M116.766923","mla":"Horsthemke, Markus, et al. “Multiple Roles of Filopodial Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal of Biological Chemistry, vol. 292, no. 17, American Society for Biochemistry and Molecular Biology, 2017, pp. 7258–73, doi:10.1074/jbc.M116.766923."},"doi":"10.1074/jbc.M116.766923","date_published":"2017-04-28T00:00:00Z","date_created":"2018-12-11T11:47:49Z","page":"7258 - 7273","day":"28","publication":"Journal of Biological Chemistry","has_accepted_license":"1","year":"2017","publisher":"American Society for Biochemistry and Molecular Biology","quality_controlled":"1","oa":1},{"date_updated":"2023-02-23T12:50:09Z","ddc":["570"],"department":[{"_id":"MiSi"},{"_id":"Bio"},{"_id":"EM-Fac"}],"file_date_updated":"2020-07-14T12:47:38Z","_id":"672","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"type":"journal_article","pubrep_id":"900","status":"public","publication_status":"published","publication_identifier":{"issn":["22111247"]},"language":[{"iso":"eng"}],"file":[{"file_size":2248814,"date_updated":"2020-07-14T12:47:38Z","creator":"system","file_name":"IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf","date_created":"2018-12-12T10:14:54Z","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_id":"5109","checksum":"8fdddaab1f1d76a6ec9ca94dcb6b07a2"}],"ec_funded":1,"issue":"5","volume":19,"abstract":[{"text":"Trafficking cells frequently transmigrate through epithelial and endothelial monolayers. How monolayers cooperate with the penetrating cells to support their transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic capillaries as a model system for transendothelial migration. We find that the chemokine CCL21, which is the decisive guidance cue for intravasation, mainly localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes extracellularly enriched at the sites of endothelial cell-cell junctions. When we reconstitute the transmigration process in vitro, we find that secretion of CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and selective calcium chelation in lymphatic endothelium attenuates transmigration. Altogether, our data demonstrate a chemokine-mediated feedback between DCs and lymphatic endothelium, which facilitates transendothelial migration.","lang":"eng"}],"oa_version":"Published Version","scopus_import":1,"intvolume":" 19","month":"05","citation":{"ieee":"K. Vaahtomeri et al., “Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia,” Cell Reports, vol. 19, no. 5. Cell Press, pp. 902–909, 2017.","short":"K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling, W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909.","apa":"Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling, M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.027","ama":"Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 2017;19(5):902-909. doi:10.1016/j.celrep.2017.04.027","mla":"Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports, vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:10.1016/j.celrep.2017.04.027.","ista":"Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909.","chicago":"Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.027."},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"Yes","publist_id":"7052","author":[{"id":"368EE576-F248-11E8-B48F-1D18A9856A87","first_name":"Kari","full_name":"Vaahtomeri, Kari","orcid":"0000-0001-7829-3518","last_name":"Vaahtomeri"},{"last_name":"Brown","full_name":"Brown, Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","first_name":"Markus"},{"orcid":"0000-0001-9843-3522","full_name":"Hauschild, Robert","last_name":"Hauschild","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","first_name":"Robert"},{"last_name":"De Vries","full_name":"De Vries, Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid"},{"last_name":"Leithner","full_name":"Leithner, Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander F"},{"full_name":"Mehling, Matthias","orcid":"0000-0001-8599-1226","last_name":"Mehling","first_name":"Matthias","id":"3C23B994-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Walter","id":"3F99E422-F248-11E8-B48F-1D18A9856A87","last_name":"Kaufmann","full_name":"Kaufmann, Walter","orcid":"0000-0001-9735-5315"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}],"title":"Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia","project":[{"call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556"},{"grant_number":"Y 564-B12","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","call_identifier":"FWF","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425"}],"year":"2017","has_accepted_license":"1","publication":"Cell Reports","day":"02","page":"902 - 909","date_created":"2018-12-11T11:47:50Z","date_published":"2017-05-02T00:00:00Z","doi":"10.1016/j.celrep.2017.04.027","oa":1,"publisher":"Cell Press","quality_controlled":"1"},{"type":"journal_article","status":"public","_id":"674","department":[{"_id":"MiSi"},{"_id":"Bio"},{"_id":"NanoFab"}],"date_updated":"2023-02-23T12:50:44Z","scopus_import":1,"intvolume":" 27","month":"05","abstract":[{"lang":"eng","text":"Navigation of cells along gradients of guidance cues is a determining step in many developmental and immunological processes. Gradients can either be soluble or immobilized to tissues as demonstrated for the haptotactic migration of dendritic cells (DCs) toward higher concentrations of immobilized chemokine CCL21. To elucidate how gradient characteristics govern cellular response patterns, we here introduce an in vitro system allowing to track migratory responses of DCs to precisely controlled immobilized gradients of CCL21. We find that haptotactic sensing depends on the absolute CCL21 concentration and local steepness of the gradient, consistent with a scenario where DC directionality is governed by the signal-to-noise ratio of CCL21 binding to the receptor CCR7. We find that the conditions for optimal DC guidance are perfectly provided by the CCL21 gradients we measure in vivo. Furthermore, we find that CCR7 signal termination by the G-protein-coupled receptor kinase 6 (GRK6) is crucial for haptotactic but dispensable for chemotactic CCL21 gradient sensing in vitro and confirm those observations in vivo. These findings suggest that stable, tissue-bound CCL21 gradients as sustainable “roads” ensure optimal guidance in vivo."}],"oa_version":"None","ec_funded":1,"volume":27,"issue":"9","publication_status":"published","publication_identifier":{"issn":["09609822"]},"language":[{"iso":"eng"}],"project":[{"grant_number":"291734","name":"International IST Postdoc Fellowship Programme","call_identifier":"FP7","_id":"25681D80-B435-11E9-9278-68D0E5697425"},{"name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12","call_identifier":"FWF","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425"}],"author":[{"id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","first_name":"Jan","full_name":"Schwarz, Jan","last_name":"Schwarz"},{"full_name":"Bierbaum, Veronika","last_name":"Bierbaum","id":"3FD04378-F248-11E8-B48F-1D18A9856A87","first_name":"Veronika"},{"id":"368EE576-F248-11E8-B48F-1D18A9856A87","first_name":"Kari","full_name":"Vaahtomeri, Kari","orcid":"0000-0001-7829-3518","last_name":"Vaahtomeri"},{"last_name":"Hauschild","orcid":"0000-0001-9843-3522","full_name":"Hauschild, Robert","first_name":"Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Brown","full_name":"Brown, Markus","first_name":"Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87"},{"last_name":"De Vries","full_name":"De Vries, Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid"},{"full_name":"Leithner, Alexander F","last_name":"Leithner","first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Anne","id":"35B76592-F248-11E8-B48F-1D18A9856A87","last_name":"Reversat","full_name":"Reversat, Anne","orcid":"0000-0003-0666-8928"},{"full_name":"Merrin, Jack","orcid":"0000-0001-5145-4609","last_name":"Merrin","first_name":"Jack","id":"4515C308-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Tarrant","full_name":"Tarrant, Teresa","first_name":"Teresa"},{"last_name":"Bollenbach","full_name":"Bollenbach, Tobias","orcid":"0000-0003-4398-476X","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","first_name":"Tobias"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt"}],"publist_id":"7050","title":"Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6","citation":{"ista":"Schwarz J, Bierbaum V, Vaahtomeri K, Hauschild R, Brown M, de Vries I, Leithner AF, Reversat A, Merrin J, Tarrant T, Bollenbach MT, Sixt MK. 2017. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. 27(9), 1314–1325.","chicago":"Schwarz, Jan, Veronika Bierbaum, Kari Vaahtomeri, Robert Hauschild, Markus Brown, Ingrid de Vries, Alexander F Leithner, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2017.04.004.","short":"J. Schwarz, V. Bierbaum, K. Vaahtomeri, R. Hauschild, M. Brown, I. de Vries, A.F. Leithner, A. Reversat, J. Merrin, T. Tarrant, M.T. Bollenbach, M.K. Sixt, Current Biology 27 (2017) 1314–1325.","ieee":"J. Schwarz et al., “Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6,” Current Biology, vol. 27, no. 9. Cell Press, pp. 1314–1325, 2017.","ama":"Schwarz J, Bierbaum V, Vaahtomeri K, et al. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. 2017;27(9):1314-1325. doi:10.1016/j.cub.2017.04.004","apa":"Schwarz, J., Bierbaum, V., Vaahtomeri, K., Hauschild, R., Brown, M., de Vries, I., … Sixt, M. K. (2017). Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2017.04.004","mla":"Schwarz, Jan, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current Biology, vol. 27, no. 9, Cell Press, 2017, pp. 1314–25, doi:10.1016/j.cub.2017.04.004."},"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","publisher":"Cell Press","quality_controlled":"1","page":"1314 - 1325","date_created":"2018-12-11T11:47:51Z","date_published":"2017-05-09T00:00:00Z","doi":"10.1016/j.cub.2017.04.004","year":"2017","publication":"Current Biology","day":"09"},{"oa_version":"Published Version","abstract":[{"text":"The INO80 complex (INO80-C) is an evolutionarily conserved nucleosome remodeler that acts in transcription, replication, and genome stability. It is required for resistance against genotoxic agents and is involved in the repair of DNA double-strand breaks (DSBs) by homologous recombination (HR). However, the causes of the HR defect in INO80-C mutant cells are controversial. Here, we unite previous findings using a system to study HR with high spatial resolution in budding yeast. We find that INO80-C has at least two distinct functions during HR—DNA end resection and presynaptic filament formation. Importantly, the second function is linked to the histone variant H2A.Z. In the absence of H2A.Z, presynaptic filament formation and HR are restored in INO80-C-deficient mutants, suggesting that presynaptic filament formation is the crucial INO80-C function during HR.","lang":"eng"}],"month":"05","intvolume":" 19","scopus_import":1,"file":[{"checksum":"efc7287d9c6354983cb151880e9ad72a","file_id":"5171","content_type":"application/pdf","access_level":"open_access","relation":"main_file","date_created":"2018-12-12T10:15:48Z","file_name":"IST-2017-899-v1+1_1-s2.0-S2211124717305454-main.pdf","date_updated":"2020-07-14T12:47:40Z","file_size":3005610,"creator":"system"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["22111247"]},"publication_status":"published","issue":"7","volume":19,"_id":"677","status":"public","pubrep_id":"899","type":"journal_article","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"ddc":["570"],"date_updated":"2021-01-12T08:08:57Z","file_date_updated":"2020-07-14T12:47:40Z","department":[{"_id":"MiSi"}],"quality_controlled":"1","publisher":"Cell Press","oa":1,"day":"16","publication":"Cell Reports","has_accepted_license":"1","year":"2017","doi":"10.1016/j.celrep.2017.04.051","date_published":"2017-05-16T00:00:00Z","date_created":"2018-12-11T11:47:52Z","page":"1294 - 1303","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"ista":"Lademann C, Renkawitz J, Pfander B, Jentsch S. 2017. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. 19(7), 1294–1303.","chicago":"Lademann, Claudio, Jörg Renkawitz, Boris Pfander, and Stefan Jentsch. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.051.","apa":"Lademann, C., Renkawitz, J., Pfander, B., & Jentsch, S. (2017). The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.051","ama":"Lademann C, Renkawitz J, Pfander B, Jentsch S. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. 2017;19(7):1294-1303. doi:10.1016/j.celrep.2017.04.051","ieee":"C. Lademann, J. Renkawitz, B. Pfander, and S. Jentsch, “The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination,” Cell Reports, vol. 19, no. 7. Cell Press, pp. 1294–1303, 2017.","short":"C. Lademann, J. Renkawitz, B. Pfander, S. Jentsch, Cell Reports 19 (2017) 1294–1303.","mla":"Lademann, Claudio, et al. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” Cell Reports, vol. 19, no. 7, Cell Press, 2017, pp. 1294–303, doi:10.1016/j.celrep.2017.04.051."},"title":"The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination","publist_id":"7046","author":[{"full_name":"Lademann, Claudio","last_name":"Lademann","first_name":"Claudio"},{"first_name":"Jörg","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","full_name":"Renkawitz, Jörg","orcid":"0000-0003-2856-3369","last_name":"Renkawitz"},{"first_name":"Boris","full_name":"Pfander, Boris","last_name":"Pfander"},{"last_name":"Jentsch","full_name":"Jentsch, Stefan","first_name":"Stefan"}]},{"external_id":{"pmid":["28515231"]},"author":[{"last_name":"Veß","full_name":"Veß, Astrid","first_name":"Astrid"},{"first_name":"Ulrich","full_name":"Blache, Ulrich","last_name":"Blache"},{"last_name":"Leitner","full_name":"Leitner, Laura","first_name":"Laura"},{"first_name":"Angela","last_name":"Kurz","full_name":"Kurz, Angela"},{"full_name":"Ehrenpfordt, Anja","last_name":"Ehrenpfordt","first_name":"Anja"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"},{"full_name":"Posern, Guido","last_name":"Posern","first_name":"Guido"}],"publist_id":"7008","title":"A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity","citation":{"mla":"Veß, Astrid, et al. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell Science, vol. 130, no. 13, Company of Biologists, 2017, pp. 2172–84, doi:10.1242/jcs.200899.","ieee":"A. Veß et al., “A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity,” Journal of Cell Science, vol. 130, no. 13. Company of Biologists, pp. 2172–2184, 2017.","short":"A. Veß, U. Blache, L. Leitner, A. Kurz, A. Ehrenpfordt, M.K. Sixt, G. Posern, Journal of Cell Science 130 (2017) 2172–2184.","ama":"Veß A, Blache U, Leitner L, et al. A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. 2017;130(13):2172-2184. doi:10.1242/jcs.200899","apa":"Veß, A., Blache, U., Leitner, L., Kurz, A., Ehrenpfordt, A., Sixt, M. K., & Posern, G. (2017). A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.200899","chicago":"Veß, Astrid, Ulrich Blache, Laura Leitner, Angela Kurz, Anja Ehrenpfordt, Michael K Sixt, and Guido Posern. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell Science. Company of Biologists, 2017. https://doi.org/10.1242/jcs.200899.","ista":"Veß A, Blache U, Leitner L, Kurz A, Ehrenpfordt A, Sixt MK, Posern G. 2017. A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. 130(13), 2172–2184."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","page":"2172 - 2184","date_created":"2018-12-11T11:47:58Z","doi":"10.1242/jcs.200899","date_published":"2017-07-01T00:00:00Z","year":"2017","has_accepted_license":"1","publication":"Journal of Cell Science","day":"01","oa":1,"quality_controlled":"1","publisher":"Company of Biologists","file_date_updated":"2020-07-14T12:47:45Z","department":[{"_id":"MiSi"}],"date_updated":"2021-01-12T08:09:41Z","ddc":["570"],"article_type":"original","type":"journal_article","status":"public","_id":"694","issue":"13","volume":130,"publication_status":"published","publication_identifier":{"issn":["00219533"]},"language":[{"iso":"eng"}],"file":[{"date_created":"2019-10-24T09:43:56Z","file_name":"2017_CellScience_Vess.pdf","creator":"dernst","date_updated":"2020-07-14T12:47:45Z","file_size":10847596,"checksum":"42c81a0a4fc3128883b391c3af3f74bc","file_id":"6966","access_level":"open_access","relation":"main_file","content_type":"application/pdf"}],"scopus_import":1,"intvolume":" 130","month":"07","abstract":[{"text":"A change regarding the extent of adhesion - hereafter referred to as adhesion plasticity - between adhesive and less-adhesive states of mammalian cells is important for their behavior. To investigate adhesion plasticity, we have selected a stable isogenic subpopulation of human MDA-MB-468 breast carcinoma cells growing in suspension. These suspension cells are unable to re-adhere to various matrices or to contract three-dimensional collagen lattices. By using transcriptome analysis, we identified the focal adhesion protein tensin3 (Tns3) as a determinant of adhesion plasticity. Tns3 is strongly reduced at mRNA and protein levels in suspension cells. Furthermore, by transiently challenging breast cancer cells to grow under non-adherent conditions markedly reduces Tns3 protein expression, which is regained upon re-adhesion. Stable knockdown of Tns3 in parental MDA-MB-468 cells results in defective adhesion, spreading and migration. Tns3-knockdown cells display impaired structure and dynamics of focal adhesion complexes as determined by immunostaining. Restoration of Tns3 protein expression in suspension cells partially rescues adhesion and focal contact composition. Our work identifies Tns3 as a crucial focal adhesion component regulated by, and functionally contributing to, the switch between adhesive and non-adhesive states in MDA-MB-468 cancer cells.","lang":"eng"}],"pmid":1,"oa_version":"Published Version"},{"quality_controlled":"1","publisher":"Cell Press","date_created":"2018-12-11T11:50:29Z","doi":"10.1016/j.cub.2016.11.035","date_published":"2017-01-09T00:00:00Z","page":"R24 - R25","publication":"Current Biology","day":"09","year":"2017","isi":1,"title":"Cell migration: Making the waves","article_processing_charge":"No","external_id":{"isi":["000391902500010"]},"publist_id":"6197","author":[{"id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D","first_name":"Jan","full_name":"Müller, Jan","last_name":"Müller"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"mla":"Müller, Jan, and Michael K. Sixt. “Cell Migration: Making the Waves.” Current Biology, vol. 27, no. 1, Cell Press, 2017, pp. R24–25, doi:10.1016/j.cub.2016.11.035.","apa":"Müller, J., & Sixt, M. K. (2017). Cell migration: Making the waves. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2016.11.035","ama":"Müller J, Sixt MK. Cell migration: Making the waves. Current Biology. 2017;27(1):R24-R25. doi:10.1016/j.cub.2016.11.035","short":"J. Müller, M.K. Sixt, Current Biology 27 (2017) R24–R25.","ieee":"J. Müller and M. K. Sixt, “Cell migration: Making the waves,” Current Biology, vol. 27, no. 1. Cell Press, pp. R24–R25, 2017.","chicago":"Müller, Jan, and Michael K Sixt. “Cell Migration: Making the Waves.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2016.11.035.","ista":"Müller J, Sixt MK. 2017. Cell migration: Making the waves. Current Biology. 27(1), R24–R25."},"intvolume":" 27","month":"01","scopus_import":"1","oa_version":"None","abstract":[{"lang":"eng","text":"Coordinated changes of cell shape are often the result of the excitable, wave-like dynamics of the actin cytoskeleton. New work shows that, in migrating cells, protrusion waves arise from mechanochemical crosstalk between adhesion sites, membrane tension and the actin protrusive machinery."}],"issue":"1","volume":27,"language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"issn":["09609822"]},"status":"public","type":"journal_article","_id":"1161","department":[{"_id":"MiSi"}],"date_updated":"2023-09-20T11:28:19Z"},{"_id":"727","status":"public","type":"journal_article","date_updated":"2023-09-28T11:33:49Z","department":[{"_id":"MiSi"},{"_id":"Bio"}],"oa_version":"None","acknowledged_ssus":[{"_id":"ScienComp"}],"abstract":[{"text":"Actin filaments polymerizing against membranes power endocytosis, vesicular traffic, and cell motility. In vitro reconstitution studies suggest that the structure and the dynamics of actin networks respond to mechanical forces. We demonstrate that lamellipodial actin of migrating cells responds to mechanical load when membrane tension is modulated. In a steady state, migrating cell filaments assume the canonical dendritic geometry, defined by Arp2/3-generated 70° branch points. Increased tension triggers a dense network with a broadened range of angles, whereas decreased tension causes a shift to a sparse configuration dominated by filaments growing perpendicularly to the plasma membrane. We show that these responses emerge from the geometry of branched actin: when load per filament decreases, elongation speed increases and perpendicular filaments gradually outcompete others because they polymerize the shortest distance to the membrane, where they are protected from capping. This network-intrinsic geometrical adaptation mechanism tunes protrusive force in response to mechanical load.","lang":"eng"}],"intvolume":" 171","month":"09","scopus_import":"1","language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"issn":["00928674"]},"ec_funded":1,"issue":"1","volume":171,"project":[{"_id":"25AD6156-B435-11E9-9278-68D0E5697425","grant_number":"LS13-029","name":"Modeling of Polarization and Motility of Leukocytes in Three-Dimensional Environments"},{"call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","grant_number":"281556","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"mla":"Mueller, Jan, et al. “Load Adaptation of Lamellipodial Actin Networks.” Cell, vol. 171, no. 1, Cell Press, 2017, pp. 188–200, doi:10.1016/j.cell.2017.07.051.","short":"J. Mueller, G. Szep, M. Nemethova, I. de Vries, A. Lieber, C. Winkler, K. Kruse, J. Small, C. Schmeiser, K. Keren, R. Hauschild, M.K. Sixt, Cell 171 (2017) 188–200.","ieee":"J. Mueller et al., “Load adaptation of lamellipodial actin networks,” Cell, vol. 171, no. 1. Cell Press, pp. 188–200, 2017.","apa":"Mueller, J., Szep, G., Nemethova, M., de Vries, I., Lieber, A., Winkler, C., … Sixt, M. K. (2017). Load adaptation of lamellipodial actin networks. Cell. Cell Press. https://doi.org/10.1016/j.cell.2017.07.051","ama":"Mueller J, Szep G, Nemethova M, et al. Load adaptation of lamellipodial actin networks. Cell. 2017;171(1):188-200. doi:10.1016/j.cell.2017.07.051","chicago":"Mueller, Jan, Gregory Szep, Maria Nemethova, Ingrid de Vries, Arnon Lieber, Christoph Winkler, Karsten Kruse, et al. “Load Adaptation of Lamellipodial Actin Networks.” Cell. Cell Press, 2017. https://doi.org/10.1016/j.cell.2017.07.051.","ista":"Mueller J, Szep G, Nemethova M, de Vries I, Lieber A, Winkler C, Kruse K, Small J, Schmeiser C, Keren K, Hauschild R, Sixt MK. 2017. Load adaptation of lamellipodial actin networks. Cell. 171(1), 188–200."},"title":"Load adaptation of lamellipodial actin networks","external_id":{"isi":["000411331800020"]},"article_processing_charge":"No","author":[{"first_name":"Jan","full_name":"Mueller, Jan","last_name":"Mueller"},{"first_name":"Gregory","id":"4BFB7762-F248-11E8-B48F-1D18A9856A87","full_name":"Szep, Gregory","last_name":"Szep"},{"first_name":"Maria","id":"34E27F1C-F248-11E8-B48F-1D18A9856A87","full_name":"Nemethova, Maria","last_name":"Nemethova"},{"id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid","last_name":"De Vries","full_name":"De Vries, Ingrid"},{"first_name":"Arnon","last_name":"Lieber","full_name":"Lieber, Arnon"},{"first_name":"Christoph","full_name":"Winkler, Christoph","last_name":"Winkler"},{"last_name":"Kruse","full_name":"Kruse, Karsten","first_name":"Karsten"},{"first_name":"John","full_name":"Small, John","last_name":"Small"},{"first_name":"Christian","full_name":"Schmeiser, Christian","last_name":"Schmeiser"},{"last_name":"Keren","full_name":"Keren, Kinneret","first_name":"Kinneret"},{"id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","first_name":"Robert","last_name":"Hauschild","orcid":"0000-0001-9843-3522","full_name":"Hauschild, Robert"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"publist_id":"6951","quality_controlled":"1","publisher":"Cell Press","publication":"Cell","day":"21","year":"2017","isi":1,"date_created":"2018-12-11T11:48:10Z","date_published":"2017-09-21T00:00:00Z","doi":"10.1016/j.cell.2017.07.051","page":"188 - 200"},{"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","ddc":["570"],"date_updated":"2024-02-21T13:47:00Z","citation":{"ieee":"A. F. Leithner, “Immunological synapse DC-Tcells.” Institute of Science and Technology Austria, 2017.","short":"A.F. Leithner, (2017).","apa":"Leithner, A. F. (2017). Immunological synapse DC-Tcells. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:71","ama":"Leithner AF. Immunological synapse DC-Tcells. 2017. doi:10.15479/AT:ISTA:71","mla":"Leithner, Alexander F. Immunological Synapse DC-Tcells. Institute of Science and Technology Austria, 2017, doi:10.15479/AT:ISTA:71.","ista":"Leithner AF. 2017. Immunological synapse DC-Tcells, Institute of Science and Technology Austria, 10.15479/AT:ISTA:71.","chicago":"Leithner, Alexander F. “Immunological Synapse DC-Tcells.” Institute of Science and Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:71."},"file_date_updated":"2020-07-14T12:47:04Z","title":"Immunological synapse DC-Tcells","department":[{"_id":"MiSi"}],"author":[{"orcid":"0000-0002-1073-744X","full_name":"Leithner, Alexander F","last_name":"Leithner","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander F"}],"article_processing_charge":"No","_id":"5567","status":"public","keyword":["Immunological synapse"],"type":"research_data","tmp":{"image":"/images/cc_0.png","legal_code_url":"https://creativecommons.org/publicdomain/zero/1.0/legalcode","name":"Creative Commons Public Domain Dedication (CC0 1.0)","short":"CC0 (1.0)"},"file":[{"access_level":"open_access","relation":"main_file","content_type":"video/x-msvideo","checksum":"3d6942d47d0737d064706b5728c4d8c8","file_id":"5612","creator":"system","date_updated":"2020-07-14T12:47:04Z","file_size":236204020,"date_created":"2018-12-12T13:02:47Z","file_name":"IST-2017-71-v1+1_Synapse_1.avi"},{"content_type":"video/x-msvideo","access_level":"open_access","relation":"main_file","checksum":"4850006c047b0147a9e85b3c2f6f0af4","file_id":"5613","date_updated":"2020-07-14T12:47:04Z","file_size":226232496,"creator":"system","date_created":"2018-12-12T13:02:51Z","file_name":"IST-2017-71-v1+2_Synapse_2.avi"}],"day":"09","has_accepted_license":"1","datarep_id":"71","year":"2017","doi":"10.15479/AT:ISTA:71","date_published":"2017-08-09T00:00:00Z","date_created":"2018-12-12T12:31:34Z","oa_version":"Published Version","abstract":[{"text":"Immunological synapse DC-Tcells","lang":"eng"}],"month":"08","publisher":"Institute of Science and Technology Austria","oa":1},{"intvolume":" 46","month":"04","quality_controlled":"1","scopus_import":1,"publisher":"Cell Press","oa_version":"None","abstract":[{"text":"Immune cells communicate using cytokine signals, but the quantitative rules of this communication aren't clear. In this issue of Immunity, Oyler-Yaniv et al. (2017) suggest that the distribution of a cytokine within a lymphatic organ is primarily governed by the local density of cells consuming it.","lang":"eng"}],"date_created":"2018-12-11T11:47:47Z","related_material":{"record":[{"status":"public","id":"6947","relation":"dissertation_contains"}]},"issue":"4","doi":"10.1016/j.immuni.2017.04.006","date_published":"2017-04-18T00:00:00Z","volume":46,"page":"519 - 520","language":[{"iso":"eng"}],"publication":"Immunity","day":"18","publication_status":"published","year":"2017","publication_identifier":{"issn":["10747613"]},"status":"public","type":"journal_article","_id":"664","title":"The dynamic cytokine niche","department":[{"_id":"MiSi"}],"publist_id":"7065","author":[{"last_name":"Assen","orcid":"0000-0003-3470-6119","full_name":"Assen, Frank P","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","first_name":"Frank P"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"}],"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","date_updated":"2024-03-27T23:30:09Z","citation":{"chicago":"Assen, Frank P, and Michael K Sixt. “The Dynamic Cytokine Niche.” Immunity. Cell Press, 2017. https://doi.org/10.1016/j.immuni.2017.04.006.","ista":"Assen FP, Sixt MK. 2017. The dynamic cytokine niche. Immunity. 46(4), 519–520.","mla":"Assen, Frank P., and Michael K. Sixt. “The Dynamic Cytokine Niche.” Immunity, vol. 46, no. 4, Cell Press, 2017, pp. 519–20, doi:10.1016/j.immuni.2017.04.006.","ieee":"F. P. Assen and M. K. Sixt, “The dynamic cytokine niche,” Immunity, vol. 46, no. 4. Cell Press, pp. 519–520, 2017.","short":"F.P. Assen, M.K. Sixt, Immunity 46 (2017) 519–520.","ama":"Assen FP, Sixt MK. The dynamic cytokine niche. Immunity. 2017;46(4):519-520. doi:10.1016/j.immuni.2017.04.006","apa":"Assen, F. P., & Sixt, M. K. (2017). The dynamic cytokine niche. Immunity. Cell Press. https://doi.org/10.1016/j.immuni.2017.04.006"}},{"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5451238/","open_access":"1"}],"scopus_import":1,"intvolume":" 127","month":"06","abstract":[{"lang":"eng","text":"Protective responses against pathogens require a rapid mobilization of resting neutrophils and the timely removal of activated ones. Neutrophils are exceptionally short-lived leukocytes, yet it remains unclear whether the lifespan of pathogen-engaged neutrophils is regulated differently from that in the circulating steady-state pool. Here, we have found that under homeostatic conditions, the mRNA-destabilizing protein tristetraprolin (TTP) regulates apoptosis and the numbers of activated infiltrating murine neutrophils but not neutrophil cellularity. Activated TTP-deficient neutrophils exhibited decreased apoptosis and enhanced accumulation at the infection site. In the context of myeloid-specific deletion of Ttp, the potentiation of neutrophil deployment protected mice against lethal soft tissue infection with Streptococcus pyogenes and prevented bacterial dissemination. Neutrophil transcriptome analysis revealed that decreased apoptosis of TTP-deficient neutrophils was specifically associated with elevated expression of myeloid cell leukemia 1 (Mcl1) but not other antiapoptotic B cell leukemia/ lymphoma 2 (Bcl2) family members. Higher Mcl1 expression resulted from stabilization of Mcl1 mRNA in the absence of TTP. The low apoptosis rate of infiltrating TTP-deficient neutrophils was comparable to that of transgenic Mcl1-overexpressing neutrophils. Our study demonstrates that posttranscriptional gene regulation by TTP schedules the termination of the antimicrobial engagement of neutrophils. The balancing role of TTP comes at the cost of an increased risk of bacterial infections."}],"oa_version":"Submitted Version","pmid":1,"issue":"6","volume":127,"related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"12401"}]},"publication_status":"published","publication_identifier":{"issn":["00219738"]},"language":[{"iso":"eng"}],"type":"journal_article","status":"public","_id":"679","department":[{"_id":"MiSi"}],"date_updated":"2024-03-27T23:30:23Z","oa":1,"quality_controlled":"1","publisher":"American Society for Clinical Investigation","acknowledgement":"This work was supported by grants from the Austrian Science Fund (FWF) (P27538-B21, I1621-B22, and SFB 43, to PK); by funding from the European Union Seventh Framework Programme Marie Curie Initial Training Networks (FP7-PEOPLE-2012-ITN) for the project INBIONET (INfection BIOlogy Training NETwork under grant agreement PITN-GA-2012-316682; and by a joint research cluster initiative of the University of Vienna and the Medical University of Vienna.","page":"2051 - 2065","date_created":"2018-12-11T11:47:53Z","date_published":"2017-06-01T00:00:00Z","doi":"10.1172/JCI80631","year":"2017","publication":"The Journal of Clinical Investigation","day":"01","project":[{"name":"The biochemical basis of PAR polarization","grant_number":"T00817-B21","call_identifier":"FWF","_id":"25985A36-B435-11E9-9278-68D0E5697425"},{"name":"Revealing the mechanisms underlying drug interactions","grant_number":"P27201-B22","call_identifier":"FWF","_id":"25E9AF9E-B435-11E9-9278-68D0E5697425"}],"external_id":{"pmid":["28504646"]},"author":[{"full_name":"Ebner, Florian","last_name":"Ebner","first_name":"Florian"},{"first_name":"Vitaly","full_name":"Sedlyarov, Vitaly","last_name":"Sedlyarov"},{"orcid":"0000-0003-1671-393X","full_name":"Tasciyan, Saren","last_name":"Tasciyan","id":"4323B49C-F248-11E8-B48F-1D18A9856A87","first_name":"Saren"},{"last_name":"Ivin","full_name":"Ivin, Masa","first_name":"Masa"},{"full_name":"Kratochvill, Franz","last_name":"Kratochvill","first_name":"Franz"},{"first_name":"Nina","full_name":"Gratz, Nina","last_name":"Gratz"},{"first_name":"Lukas","last_name":"Kenner","full_name":"Kenner, Lukas"},{"first_name":"Andreas","last_name":"Villunger","full_name":"Villunger, Andreas"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt"},{"last_name":"Kovarik","full_name":"Kovarik, Pavel","first_name":"Pavel"}],"publist_id":"7038","title":"The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection","citation":{"ista":"Ebner F, Sedlyarov V, Tasciyan S, Ivin M, Kratochvill F, Gratz N, Kenner L, Villunger A, Sixt MK, Kovarik P. 2017. The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. 127(6), 2051–2065.","chicago":"Ebner, Florian, Vitaly Sedlyarov, Saren Tasciyan, Masa Ivin, Franz Kratochvill, Nina Gratz, Lukas Kenner, Andreas Villunger, Michael K Sixt, and Pavel Kovarik. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged Neutrophils during Bacterial Infection.” The Journal of Clinical Investigation. American Society for Clinical Investigation, 2017. https://doi.org/10.1172/JCI80631.","ama":"Ebner F, Sedlyarov V, Tasciyan S, et al. The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. 2017;127(6):2051-2065. doi:10.1172/JCI80631","apa":"Ebner, F., Sedlyarov, V., Tasciyan, S., Ivin, M., Kratochvill, F., Gratz, N., … Kovarik, P. (2017). The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. American Society for Clinical Investigation. https://doi.org/10.1172/JCI80631","ieee":"F. Ebner et al., “The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection,” The Journal of Clinical Investigation, vol. 127, no. 6. American Society for Clinical Investigation, pp. 2051–2065, 2017.","short":"F. Ebner, V. Sedlyarov, S. Tasciyan, M. Ivin, F. Kratochvill, N. Gratz, L. Kenner, A. Villunger, M.K. Sixt, P. Kovarik, The Journal of Clinical Investigation 127 (2017) 2051–2065.","mla":"Ebner, Florian, et al. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged Neutrophils during Bacterial Infection.” The Journal of Clinical Investigation, vol. 127, no. 6, American Society for Clinical Investigation, 2017, pp. 2051–65, doi:10.1172/JCI80631."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87"},{"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6400263"}],"scopus_import":1,"intvolume":" 17","month":"12","abstract":[{"text":"RASGRP1 is an important guanine nucleotide exchange factor and activator of the RAS-MAPK pathway following T cell antigen receptor (TCR) signaling. The consequences of RASGRP1 mutations in humans are unknown. In a patient with recurrent bacterial and viral infections, born to healthy consanguineous parents, we used homozygosity mapping and exome sequencing to identify a biallelic stop-gain variant in RASGRP1. This variant segregated perfectly with the disease and has not been reported in genetic databases. RASGRP1 deficiency was associated in T cells and B cells with decreased phosphorylation of the extracellular-signal-regulated serine kinase ERK, which was restored following expression of wild-type RASGRP1. RASGRP1 deficiency also resulted in defective proliferation, activation and motility of T cells and B cells. RASGRP1-deficient natural killer (NK) cells exhibited impaired cytotoxicity with defective granule convergence and actin accumulation. Interaction proteomics identified the dynein light chain DYNLL1 as interacting with RASGRP1, which links RASGRP1 to cytoskeletal dynamics. RASGRP1-deficient cells showed decreased activation of the GTPase RhoA. Treatment with lenalidomide increased RhoA activity and reversed the migration and activation defects of RASGRP1-deficient lymphocytes.","lang":"eng"}],"oa_version":"Submitted Version","pmid":1,"issue":"12","volume":17,"publication_status":"published","language":[{"iso":"eng"}],"type":"journal_article","article_type":"original","status":"public","_id":"1137","department":[{"_id":"MiSi"}],"date_updated":"2021-01-12T06:48:33Z","oa":1,"quality_controlled":"1","publisher":"Nature Publishing Group","page":"1352 - 1360","date_created":"2018-12-11T11:50:21Z","date_published":"2016-12-01T00:00:00Z","doi":"10.1038/ni.3575","year":"2016","publication":"Nature Immunology","day":"01","article_processing_charge":"No","external_id":{"pmid":["27776107"]},"author":[{"first_name":"Elisabeth","last_name":"Salzer","full_name":"Salzer, Elisabeth"},{"last_name":"Çaǧdaş","full_name":"Çaǧdaş, Deniz","first_name":"Deniz"},{"last_name":"Hons","orcid":"0000-0002-6625-3348","full_name":"Hons, Miroslav","first_name":"Miroslav","id":"4167FE56-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Emily","full_name":"Mace, Emily","last_name":"Mace"},{"full_name":"Garncarz, Wojciech","last_name":"Garncarz","first_name":"Wojciech"},{"first_name":"Oezlem","last_name":"Petronczki","full_name":"Petronczki, Oezlem"},{"last_name":"Platzer","full_name":"Platzer, René","first_name":"René"},{"first_name":"Laurène","last_name":"Pfajfer","full_name":"Pfajfer, Laurène"},{"full_name":"Bilic, Ivan","last_name":"Bilic","first_name":"Ivan"},{"last_name":"Ban","full_name":"Ban, Sol","first_name":"Sol"},{"first_name":"Katharina","last_name":"Willmann","full_name":"Willmann, Katharina"},{"full_name":"Mukherjee, Malini","last_name":"Mukherjee","first_name":"Malini"},{"full_name":"Supper, Verena","last_name":"Supper","first_name":"Verena"},{"last_name":"Hsu","full_name":"Hsu, Hsiangting","first_name":"Hsiangting"},{"last_name":"Banerjee","full_name":"Banerjee, Pinaki","first_name":"Pinaki"},{"full_name":"Sinha, Papiya","last_name":"Sinha","first_name":"Papiya"},{"last_name":"Mcclanahan","full_name":"Mcclanahan, Fabienne","first_name":"Fabienne"},{"full_name":"Zlabinger, Gerhard","last_name":"Zlabinger","first_name":"Gerhard"},{"full_name":"Pickl, Winfried","last_name":"Pickl","first_name":"Winfried"},{"first_name":"John","last_name":"Gribben","full_name":"Gribben, John"},{"first_name":"Hannes","last_name":"Stockinger","full_name":"Stockinger, Hannes"},{"last_name":"Bennett","full_name":"Bennett, Keiryn","first_name":"Keiryn"},{"first_name":"Johannes","last_name":"Huppa","full_name":"Huppa, Johannes"},{"full_name":"Dupré, Loï̈C","last_name":"Dupré","first_name":"Loï̈C"},{"first_name":"Özden","last_name":"Sanal","full_name":"Sanal, Özden"},{"first_name":"Ulrich","last_name":"Jäger","full_name":"Jäger, Ulrich"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt"},{"first_name":"Ilhan","full_name":"Tezcan, Ilhan","last_name":"Tezcan"},{"first_name":"Jordan","full_name":"Orange, Jordan","last_name":"Orange"},{"first_name":"Kaan","last_name":"Boztug","full_name":"Boztug, Kaan"}],"publist_id":"6221","title":"RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics","citation":{"chicago":"Salzer, Elisabeth, Deniz Çaǧdaş, Miroslav Hons, Emily Mace, Wojciech Garncarz, Oezlem Petronczki, René Platzer, et al. “RASGRP1 Deficiency Causes Immunodeficiency with Impaired Cytoskeletal Dynamics.” Nature Immunology. Nature Publishing Group, 2016. https://doi.org/10.1038/ni.3575.","ista":"Salzer E, Çaǧdaş D, Hons M, Mace E, Garncarz W, Petronczki O, Platzer R, Pfajfer L, Bilic I, Ban S, Willmann K, Mukherjee M, Supper V, Hsu H, Banerjee P, Sinha P, Mcclanahan F, Zlabinger G, Pickl W, Gribben J, Stockinger H, Bennett K, Huppa J, Dupré L, Sanal Ö, Jäger U, Sixt MK, Tezcan I, Orange J, Boztug K. 2016. RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics. Nature Immunology. 17(12), 1352–1360.","mla":"Salzer, Elisabeth, et al. “RASGRP1 Deficiency Causes Immunodeficiency with Impaired Cytoskeletal Dynamics.” Nature Immunology, vol. 17, no. 12, Nature Publishing Group, 2016, pp. 1352–60, doi:10.1038/ni.3575.","ama":"Salzer E, Çaǧdaş D, Hons M, et al. RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics. Nature Immunology. 2016;17(12):1352-1360. doi:10.1038/ni.3575","apa":"Salzer, E., Çaǧdaş, D., Hons, M., Mace, E., Garncarz, W., Petronczki, O., … Boztug, K. (2016). RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3575","short":"E. Salzer, D. Çaǧdaş, M. Hons, E. Mace, W. Garncarz, O. Petronczki, R. Platzer, L. Pfajfer, I. Bilic, S. Ban, K. Willmann, M. Mukherjee, V. Supper, H. Hsu, P. Banerjee, P. Sinha, F. Mcclanahan, G. Zlabinger, W. Pickl, J. Gribben, H. Stockinger, K. Bennett, J. Huppa, L. Dupré, Ö. Sanal, U. Jäger, M.K. Sixt, I. Tezcan, J. Orange, K. Boztug, Nature Immunology 17 (2016) 1352–1360.","ieee":"E. Salzer et al., “RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics,” Nature Immunology, vol. 17, no. 12. Nature Publishing Group, pp. 1352–1360, 2016."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87"},{"date_updated":"2021-01-12T06:48:36Z","department":[{"_id":"MiSi"},{"_id":"PeJo"}],"_id":"1142","type":"journal_article","status":"public","publication_status":"published","language":[{"iso":"eng"}],"volume":17,"issue":"12","abstract":[{"lang":"eng","text":"Hemolysis drives susceptibility to bacterial infections and predicts poor outcome from sepsis. These detrimental effects are commonly considered to be a consequence of heme-iron serving as a nutrient for bacteria. We employed a Gram-negative sepsis model and found that elevated heme levels impaired the control of bacterial proliferation independently of heme-iron acquisition by pathogens. Heme strongly inhibited phagocytosis and the migration of human and mouse phagocytes by disrupting actin cytoskeletal dynamics via activation of the GTP-binding Rho family protein Cdc42 by the guanine nucleotide exchange factor DOCK8. A chemical screening approach revealed that quinine effectively prevented heme effects on the cytoskeleton, restored phagocytosis and improved survival in sepsis. These mechanistic insights provide potential therapeutic targets for patients with sepsis or hemolytic disorders."}],"oa_version":"Submitted Version","scopus_import":1,"main_file_link":[{"open_access":"1","url":"https://ora.ox.ac.uk/objects/uuid:f53a464e-1e5b-4f08-a7d8-b6749b852b9d"}],"month":"12","intvolume":" 17","citation":{"ista":"Martins R, Maier J, Gorki A, Huber K, Sharif O, Starkl P, Saluzzo S, Quattrone F, Gawish R, Lakovits K, Aichinger M, Radic Sarikas B, Lardeau C, Hladik A, Korosec A, Brown M, Vaahtomeri K, Duggan M, Kerjaschki D, Esterbauer H, Colinge J, Eisenbarth S, Decker T, Bennett K, Kubicek S, Sixt MK, Superti Furga G, Knapp S. 2016. Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nature Immunology. 17(12), 1361–1372.","chicago":"Martins, Rui, Julia Maier, Anna Gorki, Kilian Huber, Omar Sharif, Philipp Starkl, Simona Saluzzo, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection via Disruption of Phagocyte Functions.” Nature Immunology. Nature Publishing Group, 2016. https://doi.org/10.1038/ni.3590.","ieee":"R. Martins et al., “Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions,” Nature Immunology, vol. 17, no. 12. Nature Publishing Group, pp. 1361–1372, 2016.","short":"R. Martins, J. Maier, A. Gorki, K. Huber, O. Sharif, P. Starkl, S. Saluzzo, F. Quattrone, R. Gawish, K. Lakovits, M. Aichinger, B. Radic Sarikas, C. Lardeau, A. Hladik, A. Korosec, M. Brown, K. Vaahtomeri, M. Duggan, D. Kerjaschki, H. Esterbauer, J. Colinge, S. Eisenbarth, T. Decker, K. Bennett, S. Kubicek, M.K. Sixt, G. Superti Furga, S. Knapp, Nature Immunology 17 (2016) 1361–1372.","apa":"Martins, R., Maier, J., Gorki, A., Huber, K., Sharif, O., Starkl, P., … Knapp, S. (2016). Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3590","ama":"Martins R, Maier J, Gorki A, et al. Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nature Immunology. 2016;17(12):1361-1372. doi:10.1038/ni.3590","mla":"Martins, Rui, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection via Disruption of Phagocyte Functions.” Nature Immunology, vol. 17, no. 12, Nature Publishing Group, 2016, pp. 1361–72, doi:10.1038/ni.3590."},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","author":[{"last_name":"Martins","full_name":"Martins, Rui","first_name":"Rui"},{"full_name":"Maier, Julia","last_name":"Maier","first_name":"Julia"},{"full_name":"Gorki, Anna","last_name":"Gorki","first_name":"Anna"},{"last_name":"Huber","full_name":"Huber, Kilian","first_name":"Kilian"},{"full_name":"Sharif, Omar","last_name":"Sharif","first_name":"Omar"},{"full_name":"Starkl, Philipp","last_name":"Starkl","first_name":"Philipp"},{"first_name":"Simona","last_name":"Saluzzo","full_name":"Saluzzo, Simona"},{"full_name":"Quattrone, Federica","last_name":"Quattrone","first_name":"Federica"},{"first_name":"Riem","full_name":"Gawish, Riem","last_name":"Gawish"},{"first_name":"Karin","last_name":"Lakovits","full_name":"Lakovits, Karin"},{"first_name":"Michael","last_name":"Aichinger","full_name":"Aichinger, Michael"},{"first_name":"Branka","full_name":"Radic Sarikas, Branka","last_name":"Radic Sarikas"},{"full_name":"Lardeau, Charles","last_name":"Lardeau","first_name":"Charles"},{"first_name":"Anastasiya","last_name":"Hladik","full_name":"Hladik, Anastasiya"},{"first_name":"Ana","full_name":"Korosec, Ana","last_name":"Korosec"},{"first_name":"Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","full_name":"Brown, Markus","last_name":"Brown"},{"first_name":"Kari","id":"368EE576-F248-11E8-B48F-1D18A9856A87","full_name":"Vaahtomeri, Kari","orcid":"0000-0001-7829-3518","last_name":"Vaahtomeri"},{"id":"2EDEA62C-F248-11E8-B48F-1D18A9856A87","first_name":"Michelle","full_name":"Duggan, Michelle","last_name":"Duggan"},{"full_name":"Kerjaschki, Dontscho","last_name":"Kerjaschki","first_name":"Dontscho"},{"last_name":"Esterbauer","full_name":"Esterbauer, Harald","first_name":"Harald"},{"full_name":"Colinge, Jacques","last_name":"Colinge","first_name":"Jacques"},{"first_name":"Stephanie","full_name":"Eisenbarth, Stephanie","last_name":"Eisenbarth"},{"last_name":"Decker","full_name":"Decker, Thomas","first_name":"Thomas"},{"first_name":"Keiryn","last_name":"Bennett","full_name":"Bennett, Keiryn"},{"full_name":"Kubicek, Stefan","last_name":"Kubicek","first_name":"Stefan"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt"},{"first_name":"Giulio","full_name":"Superti Furga, Giulio","last_name":"Superti Furga"},{"first_name":"Sylvia","full_name":"Knapp, Sylvia","last_name":"Knapp"}],"publist_id":"6216","title":"Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions","year":"2016","day":"01","publication":"Nature Immunology","page":"1361 - 1372","date_published":"2016-12-01T00:00:00Z","doi":"10.1038/ni.3590","date_created":"2018-12-11T11:50:22Z","acknowledgement":"Y. Fukui (Medical Institute of Bioregulation, Kyushu University) and J. Stein (Theodor Kocher Institute, University of Bern) are acknowledged for providing the DOCK8 deficient bone marrow. and H. Häcker (St. Judes Children's Research Hospital) for providing the ERHBD-HoxB8-encoding retroviral construct. pSpCas9(BB)-2a-Puro (PX459) was a gift from F. Zhang (Massachusetts Institute of Technology) (Addgene plasmid # 48139) and pGRG36 was a gift from N. Craig (Johns Hopkins University School of Medicine) (Addgene plasmid # 16666). LifeAct-GFP-encoding retrovirus was kindly provided by A. Leithner (Institute of Science and Technology Austria). pSIM8 and TKC E. coli were gifts from D.L. Court (Center for Cancer Research, National Cancer Institute). We acknowledge M. Gröger and S. Rauscher for excellent technical support (Core imaging facility, Medical University of Vienna). We thank D.P. Barlow and L.R. Cheever for critical reading of the manuscript. This work was supported by the Austrian Academy of Sciences, the Science Fund of the Austrian National Bank (14107) and the Austrian Science Fund FWF (I1620-B22) in the Infect-ERA framework (to S.Knapp).","publisher":"Nature Publishing Group","quality_controlled":"1","oa":1},{"publication":"Developmental Cell","language":[{"iso":"eng"}],"day":"12","year":"2016","publication_status":"published","date_created":"2018-12-11T11:50:25Z","date_published":"2016-09-12T00:00:00Z","volume":38,"issue":"5","doi":"10.1016/j.devcel.2016.08.017","page":"448 - 450","oa_version":"None","abstract":[{"text":"When neutrophils infiltrate a site of inflammation, they have to stop at the right place to exert their effector function. In this issue of Developmental Cell, Wang et al. (2016) show that neutrophils sense reactive oxygen species via the TRPM2 channel to arrest migration at their target site. © 2016 Elsevier Inc.","lang":"eng"}],"intvolume":" 38","month":"09","scopus_import":1,"publisher":"Cell Press","quality_controlled":"1","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","citation":{"ieee":"J. Renkawitz and M. K. Sixt, “A Radical Break Restraining Neutrophil Migration,” Developmental Cell, vol. 38, no. 5. Cell Press, pp. 448–450, 2016.","short":"J. Renkawitz, M.K. Sixt, Developmental Cell 38 (2016) 448–450.","apa":"Renkawitz, J., & Sixt, M. K. (2016). A Radical Break Restraining Neutrophil Migration. Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2016.08.017","ama":"Renkawitz J, Sixt MK. A Radical Break Restraining Neutrophil Migration. Developmental Cell. 2016;38(5):448-450. doi:10.1016/j.devcel.2016.08.017","mla":"Renkawitz, Jörg, and Michael K. Sixt. “A Radical Break Restraining Neutrophil Migration.” Developmental Cell, vol. 38, no. 5, Cell Press, 2016, pp. 448–50, doi:10.1016/j.devcel.2016.08.017.","ista":"Renkawitz J, Sixt MK. 2016. A Radical Break Restraining Neutrophil Migration. Developmental Cell. 38(5), 448–450.","chicago":"Renkawitz, Jörg, and Michael K Sixt. “A Radical Break Restraining Neutrophil Migration.” Developmental Cell. Cell Press, 2016. https://doi.org/10.1016/j.devcel.2016.08.017."},"date_updated":"2021-01-12T06:48:39Z","title":"A Radical Break Restraining Neutrophil Migration","department":[{"_id":"MiSi"}],"publist_id":"6208","author":[{"id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","first_name":"Jörg","last_name":"Renkawitz","full_name":"Renkawitz, Jörg","orcid":"0000-0003-2856-3369"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt"}],"_id":"1150","status":"public","type":"journal_article"},{"title":"A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients","author":[{"id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","first_name":"Jan","full_name":"Schwarz, Jan","last_name":"Schwarz"},{"last_name":"Bierbaum","full_name":"Bierbaum, Veronika","id":"3FD04378-F248-11E8-B48F-1D18A9856A87","first_name":"Veronika"},{"id":"4515C308-F248-11E8-B48F-1D18A9856A87","first_name":"Jack","last_name":"Merrin","full_name":"Merrin, Jack","orcid":"0000-0001-5145-4609"},{"last_name":"Frank","full_name":"Frank, Tino","first_name":"Tino"},{"last_name":"Hauschild","full_name":"Hauschild, Robert","orcid":"0000-0001-9843-3522","first_name":"Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Bollenbach","full_name":"Bollenbach, Mark Tobias","orcid":"0000-0003-4398-476X","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","first_name":"Mark Tobias"},{"first_name":"Savaş","full_name":"Tay, Savaş","last_name":"Tay"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"},{"id":"3C23B994-F248-11E8-B48F-1D18A9856A87","first_name":"Matthias","full_name":"Mehling, Matthias","orcid":"0000-0001-8599-1226","last_name":"Mehling"}],"publist_id":"6204","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Schwarz, Jan, Veronika Bierbaum, Jack Merrin, Tino Frank, Robert Hauschild, Mark Tobias Bollenbach, Savaş Tay, Michael K Sixt, and Matthias Mehling. “A Microfluidic Device for Measuring Cell Migration towards Substrate Bound and Soluble Chemokine Gradients.” Scientific Reports. Nature Publishing Group, 2016. https://doi.org/10.1038/srep36440.","ista":"Schwarz J, Bierbaum V, Merrin J, Frank T, Hauschild R, Bollenbach MT, Tay S, Sixt MK, Mehling M. 2016. A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients. Scientific Reports. 6, 36440.","mla":"Schwarz, Jan, et al. “A Microfluidic Device for Measuring Cell Migration towards Substrate Bound and Soluble Chemokine Gradients.” Scientific Reports, vol. 6, 36440, Nature Publishing Group, 2016, doi:10.1038/srep36440.","short":"J. Schwarz, V. Bierbaum, J. Merrin, T. Frank, R. Hauschild, M.T. Bollenbach, S. Tay, M.K. Sixt, M. Mehling, Scientific Reports 6 (2016).","ieee":"J. Schwarz et al., “A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients,” Scientific Reports, vol. 6. Nature Publishing Group, 2016.","apa":"Schwarz, J., Bierbaum, V., Merrin, J., Frank, T., Hauschild, R., Bollenbach, M. T., … Mehling, M. (2016). A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients. Scientific Reports. Nature Publishing Group. https://doi.org/10.1038/srep36440","ama":"Schwarz J, Bierbaum V, Merrin J, et al. A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients. Scientific Reports. 2016;6. doi:10.1038/srep36440"},"project":[{"_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556"},{"name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12","call_identifier":"FWF","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425"}],"article_number":"36440","date_published":"2016-11-07T00:00:00Z","doi":"10.1038/srep36440","date_created":"2018-12-11T11:50:27Z","day":"07","publication":"Scientific Reports","has_accepted_license":"1","year":"2016","publisher":"Nature Publishing Group","quality_controlled":"1","oa":1,"acknowledgement":"This work was supported by the Swiss National Science Foundation (Ambizione fellowship; PZ00P3-154733 to M.M.), the Swiss Multiple Sclerosis Society (research support to M.M.), a fellowship from the Boehringer Ingelheim Fonds (BIF) to J.S., the European Research Council (grant ERC GA 281556) and a START award from the Austrian Science Foundation (FWF) to M.S. #BioimagingFacility","file_date_updated":"2018-12-12T10:09:32Z","department":[{"_id":"MiSi"},{"_id":"NanoFab"},{"_id":"Bio"},{"_id":"ToBo"}],"ddc":["579"],"date_updated":"2021-01-12T06:48:41Z","status":"public","pubrep_id":"744","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"_id":"1154","volume":6,"ec_funded":1,"file":[{"access_level":"open_access","relation":"main_file","content_type":"application/pdf","file_id":"4756","creator":"system","date_updated":"2018-12-12T10:09:32Z","file_size":2353456,"date_created":"2018-12-12T10:09:32Z","file_name":"IST-2017-744-v1+1_srep36440.pdf"}],"language":[{"iso":"eng"}],"publication_status":"published","month":"11","intvolume":" 6","scopus_import":1,"oa_version":"Published Version","abstract":[{"text":"Cellular locomotion is a central hallmark of eukaryotic life. It is governed by cell-extrinsic molecular factors, which can either emerge in the soluble phase or as immobilized, often adhesive ligands. To encode for direction, every cue must be present as a spatial or temporal gradient. Here, we developed a microfluidic chamber that allows measurement of cell migration in combined response to surface immobilized and soluble molecular gradients. As a proof of principle we study the response of dendritic cells to their major guidance cues, chemokines. The majority of data on chemokine gradient sensing is based on in vitro studies employing soluble gradients. Despite evidence suggesting that in vivo chemokines are often immobilized to sugar residues, limited information is available how cells respond to immobilized chemokines. We tracked migration of dendritic cells towards immobilized gradients of the chemokine CCL21 and varying superimposed soluble gradients of CCL19. Differential migratory patterns illustrate the potential of our setup to quantitatively study the competitive response to both types of gradients. Beyond chemokines our approach is broadly applicable to alternative systems of chemo- and haptotaxis such as cells migrating along gradients of adhesion receptor ligands vs. any soluble cue. \r\n","lang":"eng"}]},{"status":"public","type":"journal_article","_id":"1201","title":"Formin’ a nuclear protection","department":[{"_id":"MiSi"}],"publist_id":"6149","author":[{"first_name":"Jörg","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","full_name":"Renkawitz, Jörg","orcid":"0000-0003-2856-3369","last_name":"Renkawitz"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}],"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Renkawitz, Jörg, and Michael K Sixt. “Formin’ a Nuclear Protection.” Cell. Cell Press, 2016. https://doi.org/10.1016/j.cell.2016.11.024.","ista":"Renkawitz J, Sixt MK. 2016. Formin’ a nuclear protection. Cell. 167(6), 1448–1449.","mla":"Renkawitz, Jörg, and Michael K. Sixt. “Formin’ a Nuclear Protection.” Cell, vol. 167, no. 6, Cell Press, 2016, pp. 1448–49, doi:10.1016/j.cell.2016.11.024.","ama":"Renkawitz J, Sixt MK. Formin’ a nuclear protection. Cell. 2016;167(6):1448-1449. doi:10.1016/j.cell.2016.11.024","apa":"Renkawitz, J., & Sixt, M. K. (2016). Formin’ a nuclear protection. Cell. Cell Press. https://doi.org/10.1016/j.cell.2016.11.024","short":"J. Renkawitz, M.K. Sixt, Cell 167 (2016) 1448–1449.","ieee":"J. Renkawitz and M. K. Sixt, “Formin’ a nuclear protection,” Cell, vol. 167, no. 6. Cell Press, pp. 1448–1449, 2016."},"date_updated":"2021-01-12T06:49:03Z","intvolume":" 167","month":"12","quality_controlled":"1","publisher":"Cell Press","scopus_import":1,"oa_version":"None","abstract":[{"lang":"eng","text":"In this issue of Cell, Skau et al. show that the formin FMN2 organizes a perinuclear actin cytoskeleton that protects the nucleus and its genomic content of migrating cells squeezing through small spaces."}],"date_created":"2018-12-11T11:50:41Z","doi":"10.1016/j.cell.2016.11.024","volume":167,"issue":"6","date_published":"2016-12-01T00:00:00Z","page":"1448 - 1449","publication":"Cell","language":[{"iso":"eng"}],"day":"01","year":"2016","publication_status":"published"},{"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","date_updated":"2021-01-12T06:49:09Z","citation":{"mla":"Sreeramkumar, Vinatha, et al. “Efficient T-Cell Priming and Activation Requires Signaling through Prostaglandin E2 (EP) Receptors.” Immunology and Cell Biology, vol. 94, no. 1, Nature Publishing Group, 2016, pp. 39–51, doi:10.1038/icb.2015.62.","ama":"Sreeramkumar V, Hons M, Punzón C, et al. Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors. Immunology and Cell Biology. 2016;94(1):39-51. doi:10.1038/icb.2015.62","apa":"Sreeramkumar, V., Hons, M., Punzón, C., Stein, J., Sancho, D., Fresno Forcelledo, M., & Cuesta, N. (2016). Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors. Immunology and Cell Biology. Nature Publishing Group. https://doi.org/10.1038/icb.2015.62","short":"V. Sreeramkumar, M. Hons, C. Punzón, J. Stein, D. Sancho, M. Fresno Forcelledo, N. Cuesta, Immunology and Cell Biology 94 (2016) 39–51.","ieee":"V. Sreeramkumar et al., “Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors,” Immunology and Cell Biology, vol. 94, no. 1. Nature Publishing Group, pp. 39–51, 2016.","chicago":"Sreeramkumar, Vinatha, Miroslav Hons, Carmen Punzón, Jens Stein, David Sancho, Manuel Fresno Forcelledo, and Natalia Cuesta. “Efficient T-Cell Priming and Activation Requires Signaling through Prostaglandin E2 (EP) Receptors.” Immunology and Cell Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/icb.2015.62.","ista":"Sreeramkumar V, Hons M, Punzón C, Stein J, Sancho D, Fresno Forcelledo M, Cuesta N. 2016. Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors. Immunology and Cell Biology. 94(1), 39–51."},"title":"Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors","department":[{"_id":"MiSi"}],"publist_id":"6116","author":[{"last_name":"Sreeramkumar","full_name":"Sreeramkumar, Vinatha","first_name":"Vinatha"},{"orcid":"0000-0002-6625-3348","full_name":"Hons, Miroslav","last_name":"Hons","id":"4167FE56-F248-11E8-B48F-1D18A9856A87","first_name":"Miroslav"},{"first_name":"Carmen","full_name":"Punzón, Carmen","last_name":"Punzón"},{"last_name":"Stein","full_name":"Stein, Jens","first_name":"Jens"},{"last_name":"Sancho","full_name":"Sancho, David","first_name":"David"},{"first_name":"Manuel","full_name":"Fresno Forcelledo, Manuel","last_name":"Fresno Forcelledo"},{"full_name":"Cuesta, Natalia","last_name":"Cuesta","first_name":"Natalia"}],"_id":"1217","status":"public","type":"journal_article","publication":"Immunology and Cell Biology","language":[{"iso":"eng"}],"day":"01","publication_status":"published","year":"2016","date_created":"2018-12-11T11:50:46Z","volume":94,"doi":"10.1038/icb.2015.62","issue":"1","date_published":"2016-01-01T00:00:00Z","page":"39 - 51","acknowledgement":"This manuscript has been supported by grants SAF2007-61716 and S-SAL-0159/2006 awarded by the Spanish Ministry of Science and Education and the Community of Madrid to Dr M Fresno.","oa_version":"None","abstract":[{"lang":"eng","text":"Understanding the regulation of T-cell responses during inflammation and auto-immunity is fundamental for designing efficient therapeutic strategies against immune diseases. In this regard, prostaglandin E 2 (PGE 2) is mostly considered a myeloid-derived immunosuppressive molecule. We describe for the first time that T cells secrete PGE 2 during T-cell receptor stimulation. In addition, we show that autocrine PGE 2 signaling through EP receptors is essential for optimal CD4 + T-cell activation in vitro and in vivo, and for T helper 1 (Th1) and regulatory T cell differentiation. PGE 2 was found to provide additive co-stimulatory signaling through AKT activation. Intravital multiphoton microscopy showed that triggering EP receptors in T cells is also essential for the stability of T cell-dendritic cell (DC) interactions and Th-cell accumulation in draining lymph nodes (LNs) during inflammation. We further demonstrated that blocking EP receptors in T cells during the initial phase of collagen-induced arthritis in mice resulted in a reduction of clinical arthritis. This could be attributable to defective T-cell activation, accompanied by a decline in activated and interferon-γ-producing CD4 + Th1 cells in draining LNs. In conclusion, we prove that T lymphocytes secret picomolar concentrations of PGE 2, which in turn provide additive co-stimulatory signaling, enabling T cells to attain a favorable activation threshold. PGE 2 signaling in T cells is also required for maintaining long and stable interactions with DCs within LNs. Blockade of EP receptors in vivo impairs T-cell activation and development of T cell-mediated inflammatory responses. This may have implications in various pathophysiological settings."}],"intvolume":" 94","month":"01","publisher":"Nature Publishing Group","quality_controlled":"1","scopus_import":1},{"type":"journal_article","project":[{"name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556","call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425"},{"call_identifier":"FWF","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","grant_number":"Y 564-B12","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)"}],"status":"public","_id":"1285","author":[{"first_name":"Ewa","full_name":"Paluch, Ewa","last_name":"Paluch"},{"last_name":"Aspalter","full_name":"Aspalter, Irene","first_name":"Irene"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt"}],"publist_id":"6031","title":"Focal adhesion-independent cell migration","department":[{"_id":"MiSi"}],"citation":{"mla":"Paluch, Ewa, et al. “Focal Adhesion-Independent Cell Migration.” Annual Review of Cell and Developmental Biology, vol. 32, Annual Reviews, 2016, pp. 469–90, doi:10.1146/annurev-cellbio-111315-125341.","apa":"Paluch, E., Aspalter, I., & Sixt, M. K. (2016). Focal adhesion-independent cell migration. Annual Review of Cell and Developmental Biology. Annual Reviews. https://doi.org/10.1146/annurev-cellbio-111315-125341","ama":"Paluch E, Aspalter I, Sixt MK. Focal adhesion-independent cell migration. Annual Review of Cell and Developmental Biology. 2016;32:469-490. doi:10.1146/annurev-cellbio-111315-125341","ieee":"E. Paluch, I. Aspalter, and M. K. Sixt, “Focal adhesion-independent cell migration,” Annual Review of Cell and Developmental Biology, vol. 32. Annual Reviews, pp. 469–490, 2016.","short":"E. Paluch, I. Aspalter, M.K. Sixt, Annual Review of Cell and Developmental Biology 32 (2016) 469–490.","chicago":"Paluch, Ewa, Irene Aspalter, and Michael K Sixt. “Focal Adhesion-Independent Cell Migration.” Annual Review of Cell and Developmental Biology. Annual Reviews, 2016. https://doi.org/10.1146/annurev-cellbio-111315-125341.","ista":"Paluch E, Aspalter I, Sixt MK. 2016. Focal adhesion-independent cell migration. Annual Review of Cell and Developmental Biology. 32, 469–490."},"date_updated":"2021-01-12T06:49:37Z","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publisher":"Annual Reviews","quality_controlled":"1","scopus_import":1,"intvolume":" 32","month":"10","abstract":[{"lang":"eng","text":"Cell migration is central to a multitude of physiological processes, including embryonic development, immune surveillance, and wound healing, and deregulated migration is key to cancer dissemination. Decades of investigations have uncovered many of the molecular and physical mechanisms underlying cell migration. Together with protrusion extension and cell body retraction, adhesion to the substrate via specific focal adhesion points has long been considered an essential step in cell migration. Although this is true for cells moving on two-dimensional substrates, recent studies have demonstrated that focal adhesions are not required for cells moving in three dimensions, in which confinement is sufficient to maintain a cell in contact with its substrate. Here, we review the investigations that have led to challenging the requirement of specific adhesions for migration, discuss the physical mechanisms proposed for cell body translocation during focal adhesion-independent migration, and highlight the remaining open questions for the future."}],"acknowledgement":"We would like to thank Dani Bodor for critical comments on the manuscript and Guillaume Salbreux for discussions. The authors are supported by the United Kingdom's Medical Research Council (MRC) (E.K.P. and I.M.A.; core funding to the MRC Laboratory for Molecular Cell Biology), by the European Research Council [ERC GA 311637 (E.K.P.) and ERC GA 281556 (M.S.)], and by a START award from the Austrian Science Foundation (M.S.).","oa_version":"None","page":"469 - 490","ec_funded":1,"date_created":"2018-12-11T11:51:08Z","volume":32,"doi":"10.1146/annurev-cellbio-111315-125341","date_published":"2016-10-06T00:00:00Z","year":"2016","publication_status":"published","language":[{"iso":"eng"}],"publication":"Annual Review of Cell and Developmental Biology","day":"06"},{"title":"Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels","publist_id":"5697","author":[{"last_name":"Russo","full_name":"Russo, Erica","first_name":"Erica"},{"last_name":"Teijeira","full_name":"Teijeira, Alvaro","first_name":"Alvaro"},{"last_name":"Vaahtomeri","orcid":"0000-0001-7829-3518","full_name":"Vaahtomeri, Kari","id":"368EE576-F248-11E8-B48F-1D18A9856A87","first_name":"Kari"},{"first_name":"Ann","last_name":"Willrodt","full_name":"Willrodt, Ann"},{"first_name":"Joël","full_name":"Bloch, Joël","last_name":"Bloch"},{"full_name":"Nitschké, Maximilian","last_name":"Nitschké","first_name":"Maximilian"},{"full_name":"Santambrogio, Laura","last_name":"Santambrogio","first_name":"Laura"},{"first_name":"Dontscho","last_name":"Kerjaschki","full_name":"Kerjaschki, Dontscho"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt"},{"first_name":"Cornelia","last_name":"Halin","full_name":"Halin, Cornelia"}],"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"Russo, Erica, et al. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic Cells through Afferent Lymphatic Vessels.” Cell Reports, vol. 14, no. 7, Cell Press, 2016, pp. 1723–34, doi:10.1016/j.celrep.2016.01.048.","short":"E. Russo, A. Teijeira, K. Vaahtomeri, A. Willrodt, J. Bloch, M. Nitschké, L. Santambrogio, D. Kerjaschki, M.K. Sixt, C. Halin, Cell Reports 14 (2016) 1723–1734.","ieee":"E. Russo et al., “Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels,” Cell Reports, vol. 14, no. 7. Cell Press, pp. 1723–1734, 2016.","ama":"Russo E, Teijeira A, Vaahtomeri K, et al. Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels. Cell Reports. 2016;14(7):1723-1734. doi:10.1016/j.celrep.2016.01.048","apa":"Russo, E., Teijeira, A., Vaahtomeri, K., Willrodt, A., Bloch, J., Nitschké, M., … Halin, C. (2016). Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2016.01.048","chicago":"Russo, Erica, Alvaro Teijeira, Kari Vaahtomeri, Ann Willrodt, Joël Bloch, Maximilian Nitschké, Laura Santambrogio, Dontscho Kerjaschki, Michael K Sixt, and Cornelia Halin. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic Cells through Afferent Lymphatic Vessels.” Cell Reports. Cell Press, 2016. https://doi.org/10.1016/j.celrep.2016.01.048.","ista":"Russo E, Teijeira A, Vaahtomeri K, Willrodt A, Bloch J, Nitschké M, Santambrogio L, Kerjaschki D, Sixt MK, Halin C. 2016. Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels. Cell Reports. 14(7), 1723–1734."},"doi":"10.1016/j.celrep.2016.01.048","date_published":"2016-02-23T00:00:00Z","date_created":"2018-12-11T11:52:19Z","page":"1723 - 1734","day":"23","publication":"Cell Reports","has_accepted_license":"1","year":"2016","quality_controlled":"1","publisher":"Cell Press","oa":1,"file_date_updated":"2020-07-14T12:44:58Z","department":[{"_id":"MiSi"}],"ddc":["570"],"date_updated":"2021-01-12T06:51:07Z","status":"public","pubrep_id":"515","type":"journal_article","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"_id":"1490","volume":14,"issue":"7","file":[{"checksum":"c98c1151d5f1e5ce1643a83d8d7f3c29","file_id":"4948","content_type":"application/pdf","access_level":"open_access","relation":"main_file","date_created":"2018-12-12T10:12:30Z","file_name":"IST-2016-515-v1+1_1-s2.0-S2211124716300262-main.pdf","date_updated":"2020-07-14T12:44:58Z","file_size":5489897,"creator":"system"}],"language":[{"iso":"eng"}],"publication_status":"published","month":"02","intvolume":" 14","scopus_import":1,"oa_version":"Published Version","abstract":[{"lang":"eng","text":"To induce adaptive immunity, dendritic cells (DCs) migrate through afferent lymphatic vessels (LVs) to draining lymph nodes (dLNs). This process occurs in several consecutive steps. Upon entry into lymphatic capillaries, DCs first actively crawl into downstream collecting vessels. From there, they are next passively and rapidly transported to the dLN by lymph flow. Here, we describe a role for the chemokine CCL21 in intralymphatic DC crawling. Performing time-lapse imaging in murine skin, we found that blockade of CCL21-but not the absence of lymph flow-completely abolished DC migration from capillaries toward collecting vessels and reduced the ability of intralymphatic DCs to emigrate from skin. Moreover, we found that in vitro low laminar flow established a CCL21 gradient along lymphatic endothelial monolayers, thereby inducing downstream-directed DC migration. These findings reveal a role for intralymphatic CCL21 in promoting DC trafficking to dLNs, through the formation of a flow-induced gradient."}]},{"publication_status":"published","language":[{"iso":"eng"}],"ec_funded":1,"volume":351,"issue":"6269","acknowledged_ssus":[{"_id":"SSU"}],"abstract":[{"lang":"eng","text":"The addition of polysialic acid to N- and/or O-linked glycans, referred to as polysialylation, is a rare posttranslational modification that is mainly known to control the developmental plasticity of the nervous system. Here we show that CCR7, the central chemokine receptor controlling immune cell trafficking to secondary lymphatic organs, carries polysialic acid. This modification is essential for the recognition of the CCR7 ligand CCL21. As a consequence, dendritic cell trafficking is abrogated in polysialyltransferase-deficient mice, manifesting as disturbed lymph node homeostasis and unresponsiveness to inflammatory stimuli. Structure-function analysis of chemokine-receptor interactions reveals that CCL21 adopts an autoinhibited conformation, which is released upon interaction with polysialic acid. Thus, we describe a glycosylation-mediated immune cell trafficking disorder and its mechanistic basis.\r\n"}],"oa_version":"Submitted Version","pmid":1,"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5583642/","open_access":"1"}],"scopus_import":1,"intvolume":" 351","month":"01","date_updated":"2021-01-12T06:51:52Z","department":[{"_id":"MiSi"}],"_id":"1599","type":"journal_article","article_type":"original","status":"public","year":"2016","publication":"Science","day":"08","page":"186 - 190","date_created":"2018-12-11T11:52:57Z","doi":"10.1126/science.aad0512","date_published":"2016-01-08T00:00:00Z","acknowledgement":"We thank S. Schüchner and E. Ogris for kindly providing the antibody to GFP, M. Helmbrecht and A. Huber for providing Nrp2−/− mice, the IST Scientific Support Facilities for excellent services, and J. Renkawitz and K. Vaahtomeri for critically reading the manuscript. ","oa":1,"publisher":"American Association for the Advancement of Science","quality_controlled":"1","citation":{"short":"E. Kiermaier, C. Moussion, C. Veldkamp, R. Gerardy Schahn, I. de Vries, L. Williams, G. Chaffee, A. Phillips, F. Freiberger, R. Imre, D. Taleski, R. Payne, A. Braun, R. Förster, K. Mechtler, M. Mühlenhoff, B. Volkman, M.K. Sixt, Science 351 (2016) 186–190.","ieee":"E. Kiermaier et al., “Polysialylation controls dendritic cell trafficking by regulating chemokine recognition,” Science, vol. 351, no. 6269. American Association for the Advancement of Science, pp. 186–190, 2016.","apa":"Kiermaier, E., Moussion, C., Veldkamp, C., Gerardy Schahn, R., de Vries, I., Williams, L., … Sixt, M. K. (2016). Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.aad0512","ama":"Kiermaier E, Moussion C, Veldkamp C, et al. Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. Science. 2016;351(6269):186-190. doi:10.1126/science.aad0512","mla":"Kiermaier, Eva, et al. “Polysialylation Controls Dendritic Cell Trafficking by Regulating Chemokine Recognition.” Science, vol. 351, no. 6269, American Association for the Advancement of Science, 2016, pp. 186–90, doi:10.1126/science.aad0512.","ista":"Kiermaier E, Moussion C, Veldkamp C, Gerardy Schahn R, de Vries I, Williams L, Chaffee G, Phillips A, Freiberger F, Imre R, Taleski D, Payne R, Braun A, Förster R, Mechtler K, Mühlenhoff M, Volkman B, Sixt MK. 2016. Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. Science. 351(6269), 186–190.","chicago":"Kiermaier, Eva, Christine Moussion, Christopher Veldkamp, Rita Gerardy Schahn, Ingrid de Vries, Larry Williams, Gary Chaffee, et al. “Polysialylation Controls Dendritic Cell Trafficking by Regulating Chemokine Recognition.” Science. American Association for the Advancement of Science, 2016. https://doi.org/10.1126/science.aad0512."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","external_id":{"pmid":["26657283"]},"publist_id":"5570","author":[{"first_name":"Eva","id":"3EB04B78-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6165-5738","full_name":"Kiermaier, Eva","last_name":"Kiermaier"},{"id":"3356F664-F248-11E8-B48F-1D18A9856A87","first_name":"Christine","full_name":"Moussion, Christine","last_name":"Moussion"},{"full_name":"Veldkamp, Christopher","last_name":"Veldkamp","first_name":"Christopher"},{"full_name":"Gerardy Schahn, Rita","last_name":"Gerardy Schahn","first_name":"Rita"},{"id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid","full_name":"De Vries, Ingrid","last_name":"De Vries"},{"last_name":"Williams","full_name":"Williams, Larry","first_name":"Larry"},{"first_name":"Gary","last_name":"Chaffee","full_name":"Chaffee, Gary"},{"first_name":"Andrew","full_name":"Phillips, Andrew","last_name":"Phillips"},{"first_name":"Friedrich","last_name":"Freiberger","full_name":"Freiberger, Friedrich"},{"first_name":"Richard","full_name":"Imre, Richard","last_name":"Imre"},{"full_name":"Taleski, Deni","last_name":"Taleski","first_name":"Deni"},{"first_name":"Richard","full_name":"Payne, Richard","last_name":"Payne"},{"full_name":"Braun, Asolina","last_name":"Braun","first_name":"Asolina"},{"first_name":"Reinhold","full_name":"Förster, Reinhold","last_name":"Förster"},{"full_name":"Mechtler, Karl","last_name":"Mechtler","first_name":"Karl"},{"full_name":"Mühlenhoff, Martina","last_name":"Mühlenhoff","first_name":"Martina"},{"first_name":"Brian","last_name":"Volkman","full_name":"Volkman, Brian"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt"}],"title":"Polysialylation controls dendritic cell trafficking by regulating chemokine recognition","project":[{"grant_number":"281556","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425"},{"_id":"25A76F58-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Stromal Cell-immune Cell Interactions in Health and Disease","grant_number":"289720"},{"call_identifier":"FWF","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12"}]},{"date_updated":"2021-01-12T06:51:51Z","department":[{"_id":"MiSi"}],"_id":"1597","status":"public","type":"journal_article","article_type":"original","language":[{"iso":"eng"}],"publication_status":"published","volume":570,"ec_funded":1,"pmid":1,"oa_version":"None","abstract":[{"lang":"eng","text":"Chemokines are the main guidance cues directing leukocyte migration. Opposed to early assumptions, chemokines do not necessarily act as soluble cues but are often immobilized within tissues, e.g., dendritic cell migration toward lymphatic vessels is guided by a haptotactic gradient of the chemokine CCL21. Controlled assay systems to quantitatively study haptotaxis in vitro are still missing. In this chapter, we describe an in vitro haptotaxis assay optimized for the unique properties of dendritic cells. The chemokine CCL21 is immobilized in a bioactive state, using laser-assisted protein adsorption by photobleaching. The cells follow this immobilized CCL21 gradient in a haptotaxis chamber, which provides three dimensionally confined migration conditions."}],"acknowledged_ssus":[{"_id":"Bio"}],"month":"01","intvolume":" 570","scopus_import":1,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"ieee":"J. Schwarz and M. K. Sixt, “Quantitative analysis of dendritic cell haptotaxis,” Methods in Enzymology, vol. 570. Elsevier, pp. 567–581, 2016.","short":"J. Schwarz, M.K. Sixt, Methods in Enzymology 570 (2016) 567–581.","apa":"Schwarz, J., & Sixt, M. K. (2016). Quantitative analysis of dendritic cell haptotaxis. Methods in Enzymology. Elsevier. https://doi.org/10.1016/bs.mie.2015.11.004","ama":"Schwarz J, Sixt MK. Quantitative analysis of dendritic cell haptotaxis. Methods in Enzymology. 2016;570:567-581. doi:10.1016/bs.mie.2015.11.004","mla":"Schwarz, Jan, and Michael K. Sixt. “Quantitative Analysis of Dendritic Cell Haptotaxis.” Methods in Enzymology, vol. 570, Elsevier, 2016, pp. 567–81, doi:10.1016/bs.mie.2015.11.004.","ista":"Schwarz J, Sixt MK. 2016. Quantitative analysis of dendritic cell haptotaxis. Methods in Enzymology. 570, 567–581.","chicago":"Schwarz, Jan, and Michael K Sixt. “Quantitative Analysis of Dendritic Cell Haptotaxis.” Methods in Enzymology. Elsevier, 2016. https://doi.org/10.1016/bs.mie.2015.11.004."},"title":"Quantitative analysis of dendritic cell haptotaxis","publist_id":"5573","author":[{"last_name":"Schwarz","full_name":"Schwarz, Jan","first_name":"Jan","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"}],"article_processing_charge":"No","external_id":{"pmid":["26921962"]},"project":[{"_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556"},{"_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12"}],"day":"01","publication":"Methods in Enzymology","year":"2016","date_published":"2016-01-01T00:00:00Z","doi":"10.1016/bs.mie.2015.11.004","date_created":"2018-12-11T11:52:56Z","page":"567 - 581","acknowledgement":"This work was supported by the Boehringer Ingelheim Fonds, the European Research Council (ERC StG 281556), and a START Award of the Austrian Science Foundation (FWF). We thank Robert Hauschild, Anne Reversat, and Jack Merrin for valuable input and the Imaging Facility of IST Austria for excellent support.","publisher":"Elsevier","quality_controlled":"1"},{"title":"Quantitative analysis of haptotactic cell migration","publist_id":"6231","author":[{"last_name":"Schwarz","full_name":"Schwarz, Jan","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","first_name":"Jan"}],"article_processing_charge":"No","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"ista":"Schwarz J. 2016. Quantitative analysis of haptotactic cell migration. Institute of Science and Technology Austria.","chicago":"Schwarz, Jan. “Quantitative Analysis of Haptotactic Cell Migration.” Institute of Science and Technology Austria, 2016.","apa":"Schwarz, J. (2016). Quantitative analysis of haptotactic cell migration. Institute of Science and Technology Austria.","ama":"Schwarz J. Quantitative analysis of haptotactic cell migration. 2016.","short":"J. Schwarz, Quantitative Analysis of Haptotactic Cell Migration, Institute of Science and Technology Austria, 2016.","ieee":"J. Schwarz, “Quantitative analysis of haptotactic cell migration,” Institute of Science and Technology Austria, 2016.","mla":"Schwarz, Jan. Quantitative Analysis of Haptotactic Cell Migration. Institute of Science and Technology Austria, 2016."},"date_published":"2016-07-01T00:00:00Z","date_created":"2018-12-11T11:50:18Z","page":"178","day":"01","has_accepted_license":"1","year":"2016","publisher":"Institute of Science and Technology Austria","oa":1,"acknowledgement":"First, I would like to thank Michael Sixt for being a great supervisor, mentor and\r\nscientist. I highly appreciate his guidance and continued support. Furthermore, I\r\nam very grateful that he gave me the exceptional opportunity to pursue many\r\nideas of which some managed to be included in this thesis.\r\nI owe sincere thanks to the members of my PhD thesis committee, Daria\r\nSiekhaus, Daniel Legler and Harald Janovjak. Especially I would like to thank\r\nDaria for her advice and encouragement during our regular progress meetings.\r\nI also want to thank the team and fellows of the Boehringer Ingelheim Fond\r\n(BIF) PhD Fellowship for amazing and inspiring meetings and the BIF for\r\nfinancial support.\r\nImportant factors for the success of this thesis were the warm, creative\r\nand helpful atmosphere as well as the team spirit of the whole Sixt Lab.\r\nTherefore I would like to thank my current and former colleagues Frank Assen,\r\nMarkus Brown, Ingrid de Vries, Michelle Duggan, Alexander Eichner, Miroslav\r\nHons, Eva Kiermaier, Aglaja Kopf, Alexander Leithner, Christine Moussion, Jan\r\nMüller, Maria Nemethova, Jörg Renkawitz, Anne Reversat, Kari Vaahtomeri,\r\nMichele Weber and Stefan Wieser. We had an amazing time with many\r\nlegendary evenings and events. Along these lines I want to thank the in vitro\r\ncrew of the lab, Jörg, Anne and Alex, for lots of ideas and productive\r\ndiscussions. I am sure, some day we will reveal the secret of the ‘splodge’.\r\nI want to thank the members of the Heisenberg Lab for a great time and\r\nthrilling kicker matches. In this regard I especially want to thank Maurizio\r\n‘Gnocci’ Monti, Gabriel Krens, Alex Eichner, Martin Behrndt, Vanessa Barone,Philipp Schmalhorst, Michael Smutny, Daniel Capek, Anne Reversat, Eva\r\nKiermaier, Frank Assen and Jan Müller for wonderful after-lunch matches.\r\nI would not have been able to analyze the thousands of cell trajectories\r\nand probably hundreds of thousands of mouse clicks without the productive\r\ncollaboration with Veronika Bierbaum and Tobias Bollenbach. Thanks Vroni for\r\ncountless meetings, discussions and graphs and of course for proofreading and\r\nadvice for this thesis. For proofreading I also want to thank Evi, Jörg, Jack and\r\nAnne.\r\nI would like to acknowledge Matthias Mehling for a very productive\r\ncollaboration and for introducing me into the wild world of microfluidics. Jack\r\nMerrin, for countless wafers, PDMS coated coverslips and help with anything\r\nmicro-fabrication related. And Maria Nemethova for establishing the ‘click’\r\npatterning approach with me. Without her it still would be just one of the ideas…\r\nMany thanks to Ekaterina Papusheva, Robert Hauschild, Doreen Milius\r\nand Nasser Darwish from the Bioimaging Facility as well as the Preclinical and\r\nthe Life Science facilities of IST Austria for excellent technical support. At this\r\npoint I especially want to thank Robert for countless image analyses and\r\ntechnical ideas. Always interested and creative he played an essential role in all\r\nof my projects.\r\nAdditionally I want to thank Ingrid and Gabby for welcoming me warmly\r\nwhen I first started at IST, for scientific and especially mental support in all\r\nthose years, countless coffee sessions and Heurigen evenings. #BioimagingFacility #LifeScienceFacility #PreClinicalFacility","department":[{"_id":"MiSi"}],"file_date_updated":"2021-02-22T11:43:14Z","ddc":["570"],"supervisor":[{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"}],"date_updated":"2023-09-07T11:54:33Z","status":"public","type":"dissertation","_id":"1129","file":[{"checksum":"e3cd6b28f9c5cccb8891855565a2dade","file_id":"6813","relation":"main_file","access_level":"closed","content_type":"application/pdf","file_name":"Thesis_JSchwarz_final.pdf","date_created":"2019-08-13T10:55:35Z","creator":"dernst","file_size":32044069,"date_updated":"2019-08-13T10:55:35Z"},{"success":1,"checksum":"c3dbe219acf87eed2f46d21d5cca00de","file_id":"9181","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"2016_Thesis_JSchwarz.pdf","date_created":"2021-02-22T11:43:14Z","creator":"dernst","file_size":8396717,"date_updated":"2021-02-22T11:43:14Z"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2663-337X"]},"degree_awarded":"PhD","publication_status":"published","month":"07","alternative_title":["ISTA Thesis"],"oa_version":"Published Version","abstract":[{"lang":"eng","text":"Directed cell migration is a hallmark feature, present in almost all multi-cellular\r\norganisms. Despite its importance, basic questions regarding force transduction\r\nor directional sensing are still heavily investigated. Directed migration of cells\r\nguided by immobilized guidance cues - haptotaxis - occurs in key-processes,\r\nsuch as embryonic development and immunity (Middleton et al., 1997; Nguyen\r\net al., 2000; Thiery, 1984; Weber et al., 2013). Immobilized guidance cues\r\ncomprise adhesive ligands, such as collagen and fibronectin (Barczyk et al.,\r\n2009), or chemokines - the main guidance cues for migratory leukocytes\r\n(Middleton et al., 1997; Weber et al., 2013). While adhesive ligands serve as\r\nattachment sites guiding cell migration (Carter, 1965), chemokines instruct\r\nhaptotactic migration by inducing adhesion to adhesive ligands and directional\r\nguidance (Rot and Andrian, 2004; Schumann et al., 2010). Quantitative analysis\r\nof the cellular response to immobilized guidance cues requires in vitro assays\r\nthat foster cell migration, offer accurate control of the immobilized cues on a\r\nsubcellular scale and in the ideal case closely reproduce in vivo conditions. The\r\nexploration of haptotactic cell migration through design and employment of such\r\nassays represents the main focus of this work.\r\nDendritic cells (DCs) are leukocytes, which after encountering danger\r\nsignals such as pathogens in peripheral organs instruct naïve T-cells and\r\nconsequently the adaptive immune response in the lymph node (Mellman and\r\nSteinman, 2001). To reach the lymph node from the periphery, DCs follow\r\nhaptotactic gradients of the chemokine CCL21 towards lymphatic vessels\r\n(Weber et al., 2013). Questions about how DCs interpret haptotactic CCL21\r\ngradients have not yet been addressed. The main reason for this is the lack of\r\nan assay that offers diverse haptotactic environments, hence allowing the study\r\nof DC migration as a response to different signals of immobilized guidance cue.\r\nIn this work, we developed an in vitro assay that enables us to\r\nquantitatively assess DC haptotaxis, by combining precisely controllable\r\nchemokine photo-patterning with physically confining migration conditions. With this tool at hand, we studied the influence of CCL21 gradient properties and\r\nconcentration on DC haptotaxis. We found that haptotactic gradient sensing\r\ndepends on the absolute CCL21 concentration in combination with the local\r\nsteepness of the gradient. Our analysis suggests that the directionality of\r\nmigrating DCs is governed by the signal-to-noise ratio of CCL21 binding to its\r\nreceptor CCR7. Moreover, the haptotactic CCL21 gradient formed in vivo\r\nprovides an optimal shape for DCs to recognize haptotactic guidance cue.\r\nBy reconstitution of the CCL21 gradient in vitro we were also able to\r\nstudy the influence of CCR7 signal termination on DC haptotaxis. To this end,\r\nwe used DCs lacking the G-protein coupled receptor kinase GRK6, which is\r\nresponsible for CCL21 induced CCR7 receptor phosphorylation and\r\ndesensitization (Zidar et al., 2009). We found that CCR7 desensitization by\r\nGRK6 is crucial for maintenance of haptotactic CCL21 gradient sensing in vitro\r\nand confirm those observations in vivo.\r\nIn the context of the organism, immobilized haptotactic guidance cues\r\noften coincide and compete with soluble chemotactic guidance cues. During\r\nwound healing, fibroblasts are exposed and influenced by adhesive cues and\r\nsoluble factors at the same time (Wu et al., 2012; Wynn, 2008). Similarly,\r\nmigrating DCs are exposed to both, soluble chemokines (CCL19 and truncated\r\nCCL21) inducing chemotactic behavior as well as the immobilized CCL21. To\r\nquantitatively assess these complex coinciding immobilized and soluble\r\nguidance cues, we implemented our chemokine photo-patterning technique in a\r\nmicrofluidic system allowing for chemotactic gradient generation. To validate\r\nthe assay, we observed DC migration in competing CCL19/CCL21\r\nenvironments.\r\nAdhesiveness guided haptotaxis has been studied intensively over the\r\nlast century. However, quantitative studies leading to conceptual models are\r\nlargely missing, again due to the lack of a precisely controllable in vitro assay. A\r\nrequirement for such an in vitro assay is that it must prevent any uncontrolled\r\ncell adhesion. This can be accomplished by stable passivation of the surface. In\r\naddition, controlled adhesion must be sustainable, quantifiable and dose\r\ndependent in order to create homogenous gradients. Therefore, we developed a novel covalent photo-patterning technique satisfying all these needs. In\r\ncombination with a sustainable poly-vinyl alcohol (PVA) surface coating we\r\nwere able to generate gradients of adhesive cue to direct cell migration. This\r\napproach allowed us to characterize the haptotactic migratory behavior of\r\nzebrafish keratocytes in vitro. Furthermore, defined patterns of adhesive cue\r\nallowed us to control for cell shape and growth on a subcellular scale."}],"acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"},{"_id":"LifeSc"}]},{"ec_funded":1,"volume":18,"related_material":{"record":[{"relation":"dissertation_contains","id":"323","status":"public"}]},"language":[{"iso":"eng"}],"file":[{"checksum":"e1411cb7c99a2d9089c178a6abef25e7","file_id":"7844","access_level":"open_access","relation":"main_file","content_type":"application/pdf","date_created":"2020-05-14T16:33:46Z","file_name":"2018_NatureCell_Leithner.pdf","creator":"dernst","date_updated":"2020-07-14T12:44:43Z","file_size":4433280}],"publication_status":"published","intvolume":" 18","month":"10","scopus_import":1,"oa_version":"Submitted Version","acknowledged_ssus":[{"_id":"SSU"}],"abstract":[{"lang":"eng","text":"Most migrating cells extrude their front by the force of actin polymerization. Polymerization requires an initial nucleation step, which is mediated by factors establishing either parallel filaments in the case of filopodia or branched filaments that form the branched lamellipodial network. Branches are considered essential for regular cell motility and are initiated by the Arp2/3 complex, which in turn is activated by nucleation-promoting factors of the WASP and WAVE families. Here we employed rapid amoeboid crawling leukocytes and found that deletion of the WAVE complex eliminated actin branching and thus lamellipodia formation. The cells were left with parallel filaments at the leading edge, which translated, depending on the differentiation status of the cell, into a unipolar pointed cell shape or cells with multiple filopodia. Remarkably, unipolar cells migrated with increased speed and enormous directional persistence, while they were unable to turn towards chemotactic gradients. Cells with multiple filopodia retained chemotactic activity but their migration was progressively impaired with increasing geometrical complexity of the extracellular environment. These findings establish that diversified leading edge protrusions serve as explorative structures while they slow down actual locomotion."}],"file_date_updated":"2020-07-14T12:44:43Z","department":[{"_id":"MiSi"},{"_id":"NanoFab"},{"_id":"Bio"}],"ddc":["570"],"date_updated":"2024-03-27T23:30:16Z","status":"public","tmp":{"name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","image":"/images/cc_by_nc_sa.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","short":"CC BY-NC-SA (4.0)"},"type":"journal_article","article_type":"original","_id":"1321","date_created":"2018-12-11T11:51:21Z","date_published":"2016-10-24T00:00:00Z","doi":"10.1038/ncb3426","page":"1253 - 1259","publication":"Nature Cell Biology","day":"24","year":"2016","has_accepted_license":"1","oa":1,"quality_controlled":"1","publisher":"Nature Publishing Group","acknowledgement":"This work was supported by the German Research Foundation (DFG) Priority Program SP 1464 to T.E.B.S. and M.S., and European Research Council (ERC GA 281556) and Human Frontiers Program grants to M.S.\r\nService Units of IST Austria for excellent technical support.","title":"Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes","article_processing_charge":"No","author":[{"last_name":"Leithner","orcid":"0000-0002-1073-744X","full_name":"Leithner, Alexander F","first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87"},{"id":"4DFA52AE-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander","full_name":"Eichner, Alexander","last_name":"Eichner"},{"id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D","first_name":"Jan","last_name":"Müller","full_name":"Müller, Jan"},{"first_name":"Anne","id":"35B76592-F248-11E8-B48F-1D18A9856A87","last_name":"Reversat","full_name":"Reversat, Anne","orcid":"0000-0003-0666-8928"},{"first_name":"Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","full_name":"Brown, Markus","last_name":"Brown"},{"first_name":"Jan","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","full_name":"Schwarz, Jan","last_name":"Schwarz"},{"first_name":"Jack","id":"4515C308-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5145-4609","full_name":"Merrin, Jack","last_name":"Merrin"},{"first_name":"David","last_name":"De Gorter","full_name":"De Gorter, David"},{"first_name":"Florian","id":"48AD8942-F248-11E8-B48F-1D18A9856A87","full_name":"Schur, Florian","orcid":"0000-0003-4790-8078","last_name":"Schur"},{"first_name":"Jonathan","last_name":"Bayerl","full_name":"Bayerl, Jonathan"},{"full_name":"De Vries, Ingrid","last_name":"De Vries","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid"},{"first_name":"Stefan","id":"355AA5A0-F248-11E8-B48F-1D18A9856A87","last_name":"Wieser","full_name":"Wieser, Stefan","orcid":"0000-0002-2670-2217"},{"last_name":"Hauschild","full_name":"Hauschild, Robert","orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","first_name":"Robert"},{"last_name":"Lai","full_name":"Lai, Frank","first_name":"Frank"},{"first_name":"Markus","full_name":"Moser, Markus","last_name":"Moser"},{"first_name":"Dontscho","full_name":"Kerjaschki, Dontscho","last_name":"Kerjaschki"},{"full_name":"Rottner, Klemens","last_name":"Rottner","first_name":"Klemens"},{"first_name":"Victor","last_name":"Small","full_name":"Small, Victor"},{"first_name":"Theresia","full_name":"Stradal, Theresia","last_name":"Stradal"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt"}],"publist_id":"5949","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","citation":{"ista":"Leithner AF, Eichner A, Müller J, Reversat A, Brown M, Schwarz J, Merrin J, De Gorter D, Schur FK, Bayerl J, de Vries I, Wieser S, Hauschild R, Lai F, Moser M, Kerjaschki D, Rottner K, Small V, Stradal T, Sixt MK. 2016. Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. 18, 1253–1259.","chicago":"Leithner, Alexander F, Alexander Eichner, Jan Müller, Anne Reversat, Markus Brown, Jan Schwarz, Jack Merrin, et al. “Diversified Actin Protrusions Promote Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature Cell Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/ncb3426.","ieee":"A. F. Leithner et al., “Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes,” Nature Cell Biology, vol. 18. Nature Publishing Group, pp. 1253–1259, 2016.","short":"A.F. Leithner, A. Eichner, J. Müller, A. Reversat, M. Brown, J. Schwarz, J. Merrin, D. De Gorter, F.K. Schur, J. Bayerl, I. de Vries, S. Wieser, R. Hauschild, F. Lai, M. Moser, D. Kerjaschki, K. Rottner, V. Small, T. Stradal, M.K. Sixt, Nature Cell Biology 18 (2016) 1253–1259.","ama":"Leithner AF, Eichner A, Müller J, et al. Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. 2016;18:1253-1259. doi:10.1038/ncb3426","apa":"Leithner, A. F., Eichner, A., Müller, J., Reversat, A., Brown, M., Schwarz, J., … Sixt, M. K. (2016). Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb3426","mla":"Leithner, Alexander F., et al. “Diversified Actin Protrusions Promote Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature Cell Biology, vol. 18, Nature Publishing Group, 2016, pp. 1253–59, doi:10.1038/ncb3426."},"project":[{"_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556"}]},{"intvolume":" 12","month":"09","scopus_import":1,"publisher":"IOP Publishing Ltd.","quality_controlled":"1","oa_version":"None","abstract":[{"lang":"eng","text":"In growing cells, protein synthesis and cell growth are typically not synchronous, and, thus, protein concentrations vary over the cell division cycle. We have developed a theoretical description of genetic regulatory systems in bacteria that explicitly considers the cell division cycle to investigate its impact on gene expression. We calculate the cell-to-cell variations arising from cells being at different stages in the division cycle for unregulated genes and for basic regulatory mechanisms. These variations contribute to the extrinsic noise observed in single-cell experiments, and are most significant for proteins with short lifetimes. Negative autoregulation buffers against variation of protein concentration over the division cycle, but the effect is found to be relatively weak. Stronger buffering is achieved by an increased protein lifetime. Positive autoregulation can strongly amplify such variation if the parameters are set to values that lead to resonance-like behaviour. For cooperative positive autoregulation, the concentration variation over the division cycle diminishes the parameter region of bistability and modulates the switching times between the two stable states. The same effects are seen for a two-gene mutual-repression toggle switch. By contrast, an oscillatory circuit, the repressilator, is only weakly affected by the division cycle."}],"date_created":"2018-12-11T11:52:33Z","doi":"10.1088/1478-3975/12/6/066003","volume":12,"issue":"6","date_published":"2015-09-25T00:00:00Z","language":[{"iso":"eng"}],"publication":"Physical Biology","day":"25","year":"2015","publication_status":"published","status":"public","type":"journal_article","article_number":"066003","_id":"1530","title":"Impact of the cell division cycle on gene circuits","department":[{"_id":"MiSi"}],"author":[{"full_name":"Bierbaum, Veronika","last_name":"Bierbaum","id":"3FD04378-F248-11E8-B48F-1D18A9856A87","first_name":"Veronika"},{"first_name":"Stefan","last_name":"Klumpp","full_name":"Klumpp, Stefan"}],"publist_id":"5641","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2021-01-12T06:51:25Z","citation":{"chicago":"Bierbaum, Veronika, and Stefan Klumpp. “Impact of the Cell Division Cycle on Gene Circuits.” Physical Biology. IOP Publishing Ltd., 2015. https://doi.org/10.1088/1478-3975/12/6/066003.","ista":"Bierbaum V, Klumpp S. 2015. Impact of the cell division cycle on gene circuits. Physical Biology. 12(6), 066003.","mla":"Bierbaum, Veronika, and Stefan Klumpp. “Impact of the Cell Division Cycle on Gene Circuits.” Physical Biology, vol. 12, no. 6, 066003, IOP Publishing Ltd., 2015, doi:10.1088/1478-3975/12/6/066003.","ama":"Bierbaum V, Klumpp S. Impact of the cell division cycle on gene circuits. Physical Biology. 2015;12(6). doi:10.1088/1478-3975/12/6/066003","apa":"Bierbaum, V., & Klumpp, S. (2015). Impact of the cell division cycle on gene circuits. Physical Biology. IOP Publishing Ltd. https://doi.org/10.1088/1478-3975/12/6/066003","short":"V. Bierbaum, S. Klumpp, Physical Biology 12 (2015).","ieee":"V. Bierbaum and S. Klumpp, “Impact of the cell division cycle on gene circuits,” Physical Biology, vol. 12, no. 6. IOP Publishing Ltd., 2015."}},{"_id":"1553","project":[{"call_identifier":"FWF","_id":"2529486C-B435-11E9-9278-68D0E5697425","grant_number":"T 560-B17","name":"Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation"},{"call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556"},{"name":"Cell migration in complex environments: from in vivo experiments to theoretical models","grant_number":"RGP0058/2011","_id":"25ABD200-B435-11E9-9278-68D0E5697425"}],"status":"public","type":"journal_article","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"apa":"Maiuri, P., Rupprecht, J., Wieser, S., Ruprecht, V., Bénichou, O., Carpi, N., … Voituriez, R. (2015). Actin flows mediate a universal coupling between cell speed and cell persistence. Cell. Cell Press. https://doi.org/10.1016/j.cell.2015.01.056","ama":"Maiuri P, Rupprecht J, Wieser S, et al. Actin flows mediate a universal coupling between cell speed and cell persistence. Cell. 2015;161(2):374-386. doi:10.1016/j.cell.2015.01.056","ieee":"P. Maiuri et al., “Actin flows mediate a universal coupling between cell speed and cell persistence,” Cell, vol. 161, no. 2. Cell Press, pp. 374–386, 2015.","short":"P. Maiuri, J. Rupprecht, S. Wieser, V. Ruprecht, O. Bénichou, N. Carpi, M. Coppey, S. De Beco, N. Gov, C.-P.J. Heisenberg, C. Lage Crespo, F. Lautenschlaeger, M. Le Berre, A. Lennon Duménil, M. Raab, H. Thiam, M. Piel, M.K. Sixt, R. Voituriez, Cell 161 (2015) 374–386.","mla":"Maiuri, Paolo, et al. “Actin Flows Mediate a Universal Coupling between Cell Speed and Cell Persistence.” Cell, vol. 161, no. 2, Cell Press, 2015, pp. 374–86, doi:10.1016/j.cell.2015.01.056.","ista":"Maiuri P, Rupprecht J, Wieser S, Ruprecht V, Bénichou O, Carpi N, Coppey M, De Beco S, Gov N, Heisenberg C-PJ, Lage Crespo C, Lautenschlaeger F, Le Berre M, Lennon Duménil A, Raab M, Thiam H, Piel M, Sixt MK, Voituriez R. 2015. Actin flows mediate a universal coupling between cell speed and cell persistence. Cell. 161(2), 374–386.","chicago":"Maiuri, Paolo, Jean Rupprecht, Stefan Wieser, Verena Ruprecht, Olivier Bénichou, Nicolas Carpi, Mathieu Coppey, et al. “Actin Flows Mediate a Universal Coupling between Cell Speed and Cell Persistence.” Cell. Cell Press, 2015. https://doi.org/10.1016/j.cell.2015.01.056."},"date_updated":"2021-01-12T06:51:33Z","title":"Actin flows mediate a universal coupling between cell speed and cell persistence","department":[{"_id":"MiSi"},{"_id":"CaHe"}],"publist_id":"5618","author":[{"first_name":"Paolo","full_name":"Maiuri, Paolo","last_name":"Maiuri"},{"last_name":"Rupprecht","full_name":"Rupprecht, Jean","first_name":"Jean"},{"last_name":"Wieser","full_name":"Wieser, Stefan","orcid":"0000-0002-2670-2217","id":"355AA5A0-F248-11E8-B48F-1D18A9856A87","first_name":"Stefan"},{"last_name":"Ruprecht","orcid":"0000-0003-4088-8633","full_name":"Ruprecht, Verena","first_name":"Verena","id":"4D71A03A-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Bénichou","full_name":"Bénichou, Olivier","first_name":"Olivier"},{"first_name":"Nicolas","last_name":"Carpi","full_name":"Carpi, Nicolas"},{"first_name":"Mathieu","last_name":"Coppey","full_name":"Coppey, Mathieu"},{"first_name":"Simon","full_name":"De Beco, Simon","last_name":"De Beco"},{"first_name":"Nir","full_name":"Gov, Nir","last_name":"Gov"},{"full_name":"Heisenberg, Carl-Philipp J","orcid":"0000-0002-0912-4566","last_name":"Heisenberg","first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Carolina","full_name":"Lage Crespo, Carolina","last_name":"Lage Crespo"},{"first_name":"Franziska","last_name":"Lautenschlaeger","full_name":"Lautenschlaeger, Franziska"},{"first_name":"Maël","last_name":"Le Berre","full_name":"Le Berre, Maël"},{"first_name":"Ana","full_name":"Lennon Duménil, Ana","last_name":"Lennon Duménil"},{"first_name":"Matthew","last_name":"Raab","full_name":"Raab, Matthew"},{"full_name":"Thiam, Hawa","last_name":"Thiam","first_name":"Hawa"},{"first_name":"Matthieu","full_name":"Piel, Matthieu","last_name":"Piel"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt"},{"full_name":"Voituriez, Raphaël","last_name":"Voituriez","first_name":"Raphaël"}],"oa_version":"None","abstract":[{"lang":"eng","text":"Cell movement has essential functions in development, immunity, and cancer. Various cell migration patterns have been reported, but no general rule has emerged so far. Here, we show on the basis of experimental data in vitro and in vivo that cell persistence, which quantifies the straightness of trajectories, is robustly coupled to cell migration speed. We suggest that this universal coupling constitutes a generic law of cell migration, which originates in the advection of polarity cues by an actin cytoskeleton undergoing flows at the cellular scale. Our analysis relies on a theoretical model that we validate by measuring the persistence of cells upon modulation of actin flow speeds and upon optogenetic manipulation of the binding of an actin regulator to actin filaments. Beyond the quantitative prediction of the coupling, the model yields a generic phase diagram of cellular trajectories, which recapitulates the full range of observed migration patterns."}],"intvolume":" 161","month":"04","publisher":"Cell Press","scopus_import":1,"quality_controlled":"1","language":[{"iso":"eng"}],"publication":"Cell","day":"09","year":"2015","publication_status":"published","date_created":"2018-12-11T11:52:41Z","ec_funded":1,"date_published":"2015-04-09T00:00:00Z","issue":"2","doi":"10.1016/j.cell.2015.01.056","volume":161,"page":"374 - 386"},{"day":"01","language":[{"iso":"eng"}],"publication":"European Journal of Immunology","year":"2015","publication_status":"published","volume":45,"doi":"10.1002/eji.201545457","issue":"6","date_published":"2015-06-01T00:00:00Z","date_created":"2018-12-11T11:52:44Z","page":"1614 - 1620","oa_version":"None","abstract":[{"lang":"eng","text":"Replication-deficient recombinant adenoviruses are potent vectors for the efficient transient expression of exogenous genes in resting immune cells. However, most leukocytes are refractory to efficient adenoviral transduction as they lack expression of the coxsackie/adenovirus receptor (CAR). To circumvent this obstacle, we generated the R26/CAG-CARΔ1StopF (where R26 is ROSA26 and CAG is CMV early enhancer/chicken β actin promoter) knock-in mouse line. This strain allows monitoring of in situ Cre recombinase activity through expression of CARΔ1. Simultaneously, CARΔ1 expression permits selective and highly efficient adenoviral transduction of immune cell populations, such as mast cells or T cells, directly ex vivo in bulk cultures without prior cell purification or activation. Furthermore, we show that CARΔ1 expression dramatically improves adenoviral infection of in vitro differentiated conventional and plasmacytoid dendritic cells (DCs), basophils, mast cells, as well as Hoxb8-immortalized hematopoietic progenitor cells. This novel dual function mouse strain will hence be a valuable tool to rapidly dissect the function of specific genes in leukocyte physiology."}],"month":"06","intvolume":" 45","quality_controlled":"1","publisher":"Wiley","scopus_import":1,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"Heger, Klaus, et al. “A Novel Cre Recombinase Reporter Mouse Strain Facilitates Selective and Efficient Infection of Primary Immune Cells with Adenoviral Vectors.” European Journal of Immunology, vol. 45, no. 6, Wiley, 2015, pp. 1614–20, doi:10.1002/eji.201545457.","apa":"Heger, K., Kober, M., Rieß, D., Drees, C., de Vries, I., Bertossi, A., … Schmidt Supprian, M. (2015). A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors. European Journal of Immunology. Wiley. https://doi.org/10.1002/eji.201545457","ama":"Heger K, Kober M, Rieß D, et al. A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors. European Journal of Immunology. 2015;45(6):1614-1620. doi:10.1002/eji.201545457","short":"K. Heger, M. Kober, D. Rieß, C. Drees, I. de Vries, A. Bertossi, A. Roers, M.K. Sixt, M. Schmidt Supprian, European Journal of Immunology 45 (2015) 1614–1620.","ieee":"K. Heger et al., “A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors,” European Journal of Immunology, vol. 45, no. 6. Wiley, pp. 1614–1620, 2015.","chicago":"Heger, Klaus, Maike Kober, David Rieß, Christoph Drees, Ingrid de Vries, Arianna Bertossi, Axel Roers, Michael K Sixt, and Marc Schmidt Supprian. “A Novel Cre Recombinase Reporter Mouse Strain Facilitates Selective and Efficient Infection of Primary Immune Cells with Adenoviral Vectors.” European Journal of Immunology. Wiley, 2015. https://doi.org/10.1002/eji.201545457.","ista":"Heger K, Kober M, Rieß D, Drees C, de Vries I, Bertossi A, Roers A, Sixt MK, Schmidt Supprian M. 2015. A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors. European Journal of Immunology. 45(6), 1614–1620."},"date_updated":"2021-01-12T06:51:36Z","department":[{"_id":"MiSi"}],"title":"A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors","publist_id":"5610","author":[{"first_name":"Klaus","full_name":"Heger, Klaus","last_name":"Heger"},{"full_name":"Kober, Maike","last_name":"Kober","first_name":"Maike"},{"last_name":"Rieß","full_name":"Rieß, David","first_name":"David"},{"first_name":"Christoph","last_name":"Drees","full_name":"Drees, Christoph"},{"last_name":"De Vries","full_name":"De Vries, Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid"},{"full_name":"Bertossi, Arianna","last_name":"Bertossi","first_name":"Arianna"},{"first_name":"Axel","full_name":"Roers, Axel","last_name":"Roers"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Marc","last_name":"Schmidt Supprian","full_name":"Schmidt Supprian, Marc"}],"_id":"1561","status":"public","type":"journal_article"},{"_id":"1560","type":"journal_article","status":"public","citation":{"ista":"Hons M, Sixt MK. 2015. The lymph node filter revealed. Nature Immunology. 16(4), 338–340.","chicago":"Hons, Miroslav, and Michael K Sixt. “The Lymph Node Filter Revealed.” Nature Immunology. Nature Publishing Group, 2015. https://doi.org/10.1038/ni.3126.","apa":"Hons, M., & Sixt, M. K. (2015). The lymph node filter revealed. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3126","ama":"Hons M, Sixt MK. The lymph node filter revealed. Nature Immunology. 2015;16(4):338-340. doi:10.1038/ni.3126","short":"M. Hons, M.K. Sixt, Nature Immunology 16 (2015) 338–340.","ieee":"M. Hons and M. K. Sixt, “The lymph node filter revealed,” Nature Immunology, vol. 16, no. 4. Nature Publishing Group, pp. 338–340, 2015.","mla":"Hons, Miroslav, and Michael K. Sixt. “The Lymph Node Filter Revealed.” Nature Immunology, vol. 16, no. 4, Nature Publishing Group, 2015, pp. 338–40, doi:10.1038/ni.3126."},"date_updated":"2021-01-12T06:51:36Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publist_id":"5611","author":[{"full_name":"Hons, Miroslav","orcid":"0000-0002-6625-3348","last_name":"Hons","id":"4167FE56-F248-11E8-B48F-1D18A9856A87","first_name":"Miroslav"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"department":[{"_id":"MiSi"}],"title":"The lymph node filter revealed","abstract":[{"lang":"eng","text":"Stromal cells in the subcapsular sinus of the lymph node 'decide' which cells and molecules are allowed access to the deeper parenchyma. The glycoprotein PLVAP is a crucial component of this selector function."}],"oa_version":"None","publisher":"Nature Publishing Group","quality_controlled":"1","scopus_import":1,"intvolume":" 16","month":"03","publication_status":"published","year":"2015","publication":"Nature Immunology","language":[{"iso":"eng"}],"day":"19","page":"338 - 340","date_created":"2018-12-11T11:52:43Z","doi":"10.1038/ni.3126","date_published":"2015-03-19T00:00:00Z","issue":"4","volume":16},{"_id":"1575","status":"public","pubrep_id":"476","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"ddc":["570"],"date_updated":"2021-01-12T06:51:42Z","file_date_updated":"2020-07-14T12:45:02Z","department":[{"_id":"MiSi"}],"oa_version":"Published Version","abstract":[{"lang":"eng","text":"The immune response relies on the migration of leukocytes and on their ability to stop in precise anatomical locations to fulfil their task. How leukocyte migration and function are coordinated is unknown. Here we show that in immature dendritic cells, which patrol their environment by engulfing extracellular material, cell migration and antigen capture are antagonistic. This antagonism results from transient enrichment of myosin IIA at the cell front, which disrupts the back-to-front gradient of the motor protein, slowing down locomotion but promoting antigen capture. We further highlight that myosin IIA enrichment at the cell front requires the MHC class II-associated invariant chain (Ii). Thus, by controlling myosin IIA localization, Ii imposes on dendritic cells an intermittent antigen capture behaviour that might facilitate environment patrolling. We propose that the requirement for myosin II in both cell migration and specific cell functions may provide a general mechanism for their coordination in time and space."}],"month":"06","intvolume":" 6","scopus_import":1,"file":[{"access_level":"open_access","relation":"main_file","content_type":"application/pdf","file_id":"4915","checksum":"bae12e86be2adb28253f890b8bba8315","creator":"system","date_updated":"2020-07-14T12:45:02Z","file_size":4530215,"date_created":"2018-12-12T10:11:58Z","file_name":"IST-2016-476-v1+1_ncomms8526.pdf"}],"language":[{"iso":"eng"}],"publication_status":"published","volume":6,"article_number":"7526","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"ama":"Chabaud M, Heuzé M, Bretou M, et al. Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells. Nature Communications. 2015;6. doi:10.1038/ncomms8526","apa":"Chabaud, M., Heuzé, M., Bretou, M., Vargas, P., Maiuri, P., Solanes, P., … Lennon Duménil, A. (2015). Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms8526","ieee":"M. Chabaud et al., “Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells,” Nature Communications, vol. 6. Nature Publishing Group, 2015.","short":"M. Chabaud, M. Heuzé, M. Bretou, P. Vargas, P. Maiuri, P. Solanes, M. Maurin, E. Terriac, M. Le Berre, D. Lankar, T. Piolot, R. Adelstein, Y. Zhang, M.K. Sixt, J. Jacobelli, O. Bénichou, R. Voituriez, M. Piel, A. Lennon Duménil, Nature Communications 6 (2015).","mla":"Chabaud, Mélanie, et al. “Cell Migration and Antigen Capture Are Antagonistic Processes Coupled by Myosin II in Dendritic Cells.” Nature Communications, vol. 6, 7526, Nature Publishing Group, 2015, doi:10.1038/ncomms8526.","ista":"Chabaud M, Heuzé M, Bretou M, Vargas P, Maiuri P, Solanes P, Maurin M, Terriac E, Le Berre M, Lankar D, Piolot T, Adelstein R, Zhang Y, Sixt MK, Jacobelli J, Bénichou O, Voituriez R, Piel M, Lennon Duménil A. 2015. Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells. Nature Communications. 6, 7526.","chicago":"Chabaud, Mélanie, Mélina Heuzé, Marine Bretou, Pablo Vargas, Paolo Maiuri, Paola Solanes, Mathieu Maurin, et al. “Cell Migration and Antigen Capture Are Antagonistic Processes Coupled by Myosin II in Dendritic Cells.” Nature Communications. Nature Publishing Group, 2015. https://doi.org/10.1038/ncomms8526."},"title":"Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells","publist_id":"5596","author":[{"last_name":"Chabaud","full_name":"Chabaud, Mélanie","first_name":"Mélanie"},{"first_name":"Mélina","last_name":"Heuzé","full_name":"Heuzé, Mélina"},{"first_name":"Marine","full_name":"Bretou, Marine","last_name":"Bretou"},{"full_name":"Vargas, Pablo","last_name":"Vargas","first_name":"Pablo"},{"first_name":"Paolo","full_name":"Maiuri, Paolo","last_name":"Maiuri"},{"first_name":"Paola","full_name":"Solanes, Paola","last_name":"Solanes"},{"full_name":"Maurin, Mathieu","last_name":"Maurin","first_name":"Mathieu"},{"last_name":"Terriac","full_name":"Terriac, Emmanuel","first_name":"Emmanuel"},{"full_name":"Le Berre, Maël","last_name":"Le Berre","first_name":"Maël"},{"first_name":"Danielle","full_name":"Lankar, Danielle","last_name":"Lankar"},{"full_name":"Piolot, Tristan","last_name":"Piolot","first_name":"Tristan"},{"full_name":"Adelstein, Robert","last_name":"Adelstein","first_name":"Robert"},{"first_name":"Yingfan","full_name":"Zhang, Yingfan","last_name":"Zhang"},{"last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"},{"last_name":"Jacobelli","full_name":"Jacobelli, Jordan","first_name":"Jordan"},{"first_name":"Olivier","last_name":"Bénichou","full_name":"Bénichou, Olivier"},{"last_name":"Voituriez","full_name":"Voituriez, Raphaël","first_name":"Raphaël"},{"first_name":"Matthieu","last_name":"Piel","full_name":"Piel, Matthieu"},{"last_name":"Lennon Duménil","full_name":"Lennon Duménil, Ana","first_name":"Ana"}],"acknowledgement":"M.C. and M.L.H. were supported by fellowships from the Fondation pour la Recherche Médicale and the Association pour la Recherche contre le Cancer, respectively. This work was funded by grants from the City of Paris and the European Research Council to A.-M.L.-D. (Strapacemi 243103), the Association Nationale pour la Recherche (ANR-09-PIRI-0027-PCVI) and the InnaBiosanté foundation (Micemico) to A.-M.L.-D., M.P. and R.V., and the DCBIOL Labex from the French Government (ANR-10-IDEX-0001-02-PSL* and ANR-11-LABX-0043). The super-resolution SIM microscope was funded through an ERC Advanced Investigator Grant (250367) to Edith Heard (CNRS UMR3215/Inserm U934, Institut Curie).","publisher":"Nature Publishing Group","quality_controlled":"1","oa":1,"day":"25","publication":"Nature Communications","has_accepted_license":"1","year":"2015","doi":"10.1038/ncomms8526","date_published":"2015-06-25T00:00:00Z","date_created":"2018-12-11T11:52:48Z"},{"date_updated":"2021-01-12T06:52:27Z","citation":{"chicago":"Sixt, Michael K, and Erez Raz. “Editorial Overview: Cell Adhesion and Migration.” Current Opinion in Cell Biology. Elsevier, 2015. https://doi.org/10.1016/j.ceb.2015.09.004.","ista":"Sixt MK, Raz E. 2015. Editorial overview: Cell adhesion and migration. Current Opinion in Cell Biology. 36(10), 4–6.","mla":"Sixt, Michael K., and Erez Raz. “Editorial Overview: Cell Adhesion and Migration.” Current Opinion in Cell Biology, vol. 36, no. 10, Elsevier, 2015, pp. 4–6, doi:10.1016/j.ceb.2015.09.004.","ama":"Sixt MK, Raz E. Editorial overview: Cell adhesion and migration. Current Opinion in Cell Biology. 2015;36(10):4-6. doi:10.1016/j.ceb.2015.09.004","apa":"Sixt, M. K., & Raz, E. (2015). Editorial overview: Cell adhesion and migration. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2015.09.004","ieee":"M. K. Sixt and E. Raz, “Editorial overview: Cell adhesion and migration,” Current Opinion in Cell Biology, vol. 36, no. 10. Elsevier, pp. 4–6, 2015.","short":"M.K. Sixt, E. Raz, Current Opinion in Cell Biology 36 (2015) 4–6."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179"},{"first_name":"Erez","full_name":"Raz, Erez","last_name":"Raz"}],"publist_id":"5473","title":"Editorial overview: Cell adhesion and migration","department":[{"_id":"MiSi"}],"_id":"1676","type":"journal_article","status":"public","year":"2015","publication_status":"published","publication":"Current Opinion in Cell Biology","language":[{"iso":"eng"}],"day":"01","page":"4 - 6","date_created":"2018-12-11T11:53:25Z","issue":"10","volume":36,"doi":"10.1016/j.ceb.2015.09.004","date_published":"2015-10-01T00:00:00Z","oa_version":"None","scopus_import":1,"publisher":"Elsevier","intvolume":" 36","month":"10"},{"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","pubrep_id":"445","status":"public","_id":"1687","file_date_updated":"2020-07-14T12:45:12Z","department":[{"_id":"MiSi"}],"date_updated":"2021-01-12T06:52:31Z","ddc":["570"],"scopus_import":1,"intvolume":" 36","month":"10","abstract":[{"text":"Guided cell movement is essential for development and integrity of animals and crucially involved in cellular immune responses. Leukocytes are professional migratory cells that can navigate through most types of tissues and sense a wide range of directional cues. The responses of these cells to attractants have been mainly explored in tissue culture settings. How leukocytes make directional decisions in situ, within the challenging environment of a tissue maze, is less understood. Here we review recent advances in how leukocytes sense chemical cues in complex tissue settings and make links with paradigms of directed migration in development and Dictyostelium discoideum amoebae.","lang":"eng"}],"oa_version":"Published Version","ec_funded":1,"issue":"10","volume":36,"publication_status":"published","language":[{"iso":"eng"}],"file":[{"date_created":"2018-12-12T10:11:21Z","file_name":"IST-2016-445-v1+1_1-s2.0-S0955067415001064-main.pdf","date_updated":"2020-07-14T12:45:12Z","file_size":797964,"creator":"system","file_id":"4875","checksum":"c29973924b790aab02fdd91857759cfb","content_type":"application/pdf","access_level":"open_access","relation":"main_file"}],"project":[{"call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556"}],"author":[{"first_name":"Milka","full_name":"Sarris, Milka","last_name":"Sarris"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}],"publist_id":"5458","title":"Navigating in tissue mazes: Chemoattractant interpretation in complex environments","citation":{"apa":"Sarris, M., & Sixt, M. K. (2015). Navigating in tissue mazes: Chemoattractant interpretation in complex environments. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2015.08.001","ama":"Sarris M, Sixt MK. Navigating in tissue mazes: Chemoattractant interpretation in complex environments. Current Opinion in Cell Biology. 2015;36(10):93-102. doi:10.1016/j.ceb.2015.08.001","ieee":"M. Sarris and M. K. Sixt, “Navigating in tissue mazes: Chemoattractant interpretation in complex environments,” Current Opinion in Cell Biology, vol. 36, no. 10. Elsevier, pp. 93–102, 2015.","short":"M. Sarris, M.K. Sixt, Current Opinion in Cell Biology 36 (2015) 93–102.","mla":"Sarris, Milka, and Michael K. Sixt. “Navigating in Tissue Mazes: Chemoattractant Interpretation in Complex Environments.” Current Opinion in Cell Biology, vol. 36, no. 10, Elsevier, 2015, pp. 93–102, doi:10.1016/j.ceb.2015.08.001.","ista":"Sarris M, Sixt MK. 2015. Navigating in tissue mazes: Chemoattractant interpretation in complex environments. Current Opinion in Cell Biology. 36(10), 93–102.","chicago":"Sarris, Milka, and Michael K Sixt. “Navigating in Tissue Mazes: Chemoattractant Interpretation in Complex Environments.” Current Opinion in Cell Biology. Elsevier, 2015. https://doi.org/10.1016/j.ceb.2015.08.001."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","oa":1,"quality_controlled":"1","publisher":"Elsevier","page":"93 - 102","date_created":"2018-12-11T11:53:28Z","doi":"10.1016/j.ceb.2015.08.001","date_published":"2015-10-01T00:00:00Z","year":"2015","has_accepted_license":"1","publication":"Current Opinion in Cell Biology","day":"01"},{"_id":"1686","status":"public","type":"journal_article","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2021-01-12T06:52:31Z","citation":{"ama":"Kiermaier E, Sixt MK. Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. Science. 2015;349(6252):1055-1056. doi:10.1126/science.aad0867","apa":"Kiermaier, E., & Sixt, M. K. (2015). Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.aad0867","short":"E. Kiermaier, M.K. Sixt, Science 349 (2015) 1055–1056.","ieee":"E. Kiermaier and M. K. Sixt, “Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection,” Science, vol. 349, no. 6252. American Association for the Advancement of Science, pp. 1055–1056, 2015.","mla":"Kiermaier, Eva, and Michael K. Sixt. “Fragmented Communication between Immune Cells: Neutrophils Blaze a Trail with Migratory Cues for T Cells to Follow to Sites of Infection.” Science, vol. 349, no. 6252, American Association for the Advancement of Science, 2015, pp. 1055–56, doi:10.1126/science.aad0867.","ista":"Kiermaier E, Sixt MK. 2015. Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. Science. 349(6252), 1055–1056.","chicago":"Kiermaier, Eva, and Michael K Sixt. “Fragmented Communication between Immune Cells: Neutrophils Blaze a Trail with Migratory Cues for T Cells to Follow to Sites of Infection.” Science. American Association for the Advancement of Science, 2015. https://doi.org/10.1126/science.aad0867."},"title":"Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection","department":[{"_id":"MiSi"}],"publist_id":"5459","author":[{"id":"3EB04B78-F248-11E8-B48F-1D18A9856A87","first_name":"Eva","last_name":"Kiermaier","orcid":"0000-0001-6165-5738","full_name":"Kiermaier, Eva"},{"last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}],"oa_version":"None","month":"09","intvolume":" 349","scopus_import":1,"quality_controlled":"1","publisher":"American Association for the Advancement of Science","day":"04","publication":"Science","language":[{"iso":"eng"}],"year":"2015","publication_status":"published","volume":349,"doi":"10.1126/science.aad0867","date_published":"2015-09-04T00:00:00Z","issue":"6252","date_created":"2018-12-11T11:53:28Z","page":"1055 - 1056"},{"page":"2866 - 2880","date_created":"2018-12-11T11:46:41Z","doi":"10.1242/jcs.167999","volume":128,"date_published":"2015-06-15T00:00:00Z","issue":"15","year":"2015","publication_status":"published","publication":"Journal of Cell Science","language":[{"iso":"eng"}],"day":"15","quality_controlled":"1","publisher":"Company of Biologists","scopus_import":1,"intvolume":" 128","month":"06","abstract":[{"lang":"eng","text":"Dendritic cells are potent antigen-presenting cells endowed with the unique ability to initiate adaptive immune responses upon inflammation. Inflammatory processes are often associated with an increased production of serotonin, which operates by activating specific receptors. However, the functional role of serotonin receptors in regulation of dendritic cell functions is poorly understood. Here, we demonstrate that expression of serotonin receptor 5-HT7 (5-HT7TR) as well as its downstream effector Cdc42 is upregulated in dendritic cells upon maturation. Although dendritic cell maturation was independent of 5-HT7TR, receptor stimulation affected dendritic cell morphology through Cdc42-mediated signaling. In addition, basal activity of 5-HT7TR was required for the proper expression of the chemokine receptor CCR7, which is a key factor that controls dendritic cell migration. Consistent with this, we observed that 5-HT7TR enhances chemotactic motility of dendritic cells in vitro by modulating their directionality and migration velocity. Accordingly, migration of dendritic cells in murine colon explants was abolished after pharmacological receptor inhibition. Our results indicate that there is a crucial role for 5-HT7TR-Cdc42-mediated signaling in the regulation of dendritic cell morphology and motility, suggesting that 5-HT7TR could be a new target for treatment of a variety of inflammatory and immune disorders."}],"oa_version":"None","publist_id":"7343","author":[{"first_name":"Katrin","last_name":"Holst","full_name":"Holst, Katrin"},{"full_name":"Guseva, Daria","last_name":"Guseva","first_name":"Daria"},{"full_name":"Schindler, Susann","last_name":"Schindler","first_name":"Susann"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179"},{"first_name":"Armin","last_name":"Braun","full_name":"Braun, Armin"},{"last_name":"Chopra","full_name":"Chopra, Himpriya","first_name":"Himpriya"},{"first_name":"Oliver","full_name":"Pabst, Oliver","last_name":"Pabst"},{"first_name":"Evgeni","last_name":"Ponimaskin","full_name":"Ponimaskin, Evgeni"}],"title":"The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells","department":[{"_id":"MiSi"}],"citation":{"chicago":"Holst, Katrin, Daria Guseva, Susann Schindler, Michael K Sixt, Armin Braun, Himpriya Chopra, Oliver Pabst, and Evgeni Ponimaskin. “The Serotonin Receptor 5-HT7R Regulates the Morphology and Migratory Properties of Dendritic Cells.” Journal of Cell Science. Company of Biologists, 2015. https://doi.org/10.1242/jcs.167999.","ista":"Holst K, Guseva D, Schindler S, Sixt MK, Braun A, Chopra H, Pabst O, Ponimaskin E. 2015. The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. Journal of Cell Science. 128(15), 2866–2880.","mla":"Holst, Katrin, et al. “The Serotonin Receptor 5-HT7R Regulates the Morphology and Migratory Properties of Dendritic Cells.” Journal of Cell Science, vol. 128, no. 15, Company of Biologists, 2015, pp. 2866–80, doi:10.1242/jcs.167999.","apa":"Holst, K., Guseva, D., Schindler, S., Sixt, M. K., Braun, A., Chopra, H., … Ponimaskin, E. (2015). The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.167999","ama":"Holst K, Guseva D, Schindler S, et al. The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. Journal of Cell Science. 2015;128(15):2866-2880. doi:10.1242/jcs.167999","short":"K. Holst, D. Guseva, S. Schindler, M.K. Sixt, A. Braun, H. Chopra, O. Pabst, E. Ponimaskin, Journal of Cell Science 128 (2015) 2866–2880.","ieee":"K. Holst et al., “The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells,” Journal of Cell Science, vol. 128, no. 15. Company of Biologists, pp. 2866–2880, 2015."},"date_updated":"2021-01-12T08:00:54Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","type":"journal_article","status":"public","_id":"477"},{"_id":"1618","type":"journal_article","status":"public","date_updated":"2023-03-30T11:32:57Z","department":[{"_id":"MiSi"}],"abstract":[{"text":"CCL19 and CCL21 are chemokines involved in the trafficking of immune cells, particularly within the lymphatic system, through activation of CCR7. Concurrent expression of PSGL-1 and CCR7 in naive T-cells enhances recruitment of these cells to secondary lymphoid organs by CCL19 and CCL21. Here the solution structure of CCL19 is reported. It contains a canonical chemokine domain. Chemical shift mapping shows the N-termini of PSGL-1 and CCR7 have overlapping binding sites for CCL19 and binding is competitive. Implications for the mechanism of PSGL-1's enhancement of resting T-cell recruitment are discussed.","lang":"eng"}],"pmid":1,"oa_version":"Submitted Version","scopus_import":"1","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4809050/"}],"month":"06","intvolume":" 54","publication_status":"published","language":[{"iso":"eng"}],"issue":"27","volume":54,"ec_funded":1,"project":[{"grant_number":"281556","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"}],"citation":{"chicago":"Veldkamp, Christopher, Eva Kiermaier, Skylar Gabel Eissens, Miranda Gillitzer, David Lippner, Frank Disilvio, Casey Mueller, et al. “Solution Structure of CCL19 and Identification of Overlapping CCR7 and PSGL-1 Binding Sites.” Biochemistry. American Chemical Society, 2015. https://doi.org/10.1021/acs.biochem.5b00560.","ista":"Veldkamp C, Kiermaier E, Gabel Eissens S, Gillitzer M, Lippner D, Disilvio F, Mueller C, Wantuch P, Chaffee G, Famiglietti M, Zgoba D, Bailey A, Bah Y, Engebretson S, Graupner D, Lackner E, Larosa V, Medeiros T, Olson M, Phillips A, Pyles H, Richard A, Schoeller S, Touzeau B, Williams L, Sixt MK, Peterson F. 2015. Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites. Biochemistry. 54(27), 4163–4166.","mla":"Veldkamp, Christopher, et al. “Solution Structure of CCL19 and Identification of Overlapping CCR7 and PSGL-1 Binding Sites.” Biochemistry, vol. 54, no. 27, American Chemical Society, 2015, pp. 4163–66, doi:10.1021/acs.biochem.5b00560.","ieee":"C. Veldkamp et al., “Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites,” Biochemistry, vol. 54, no. 27. American Chemical Society, pp. 4163–4166, 2015.","short":"C. Veldkamp, E. Kiermaier, S. Gabel Eissens, M. Gillitzer, D. Lippner, F. Disilvio, C. Mueller, P. Wantuch, G. Chaffee, M. Famiglietti, D. Zgoba, A. Bailey, Y. Bah, S. Engebretson, D. Graupner, E. Lackner, V. Larosa, T. Medeiros, M. Olson, A. Phillips, H. Pyles, A. Richard, S. Schoeller, B. Touzeau, L. Williams, M.K. Sixt, F. Peterson, Biochemistry 54 (2015) 4163–4166.","ama":"Veldkamp C, Kiermaier E, Gabel Eissens S, et al. Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites. Biochemistry. 2015;54(27):4163-4166. doi:10.1021/acs.biochem.5b00560","apa":"Veldkamp, C., Kiermaier, E., Gabel Eissens, S., Gillitzer, M., Lippner, D., Disilvio, F., … Peterson, F. (2015). Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites. Biochemistry. American Chemical Society. https://doi.org/10.1021/acs.biochem.5b00560"},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publist_id":"5548","author":[{"full_name":"Veldkamp, Christopher","last_name":"Veldkamp","first_name":"Christopher"},{"first_name":"Eva","id":"3EB04B78-F248-11E8-B48F-1D18A9856A87","last_name":"Kiermaier","full_name":"Kiermaier, Eva","orcid":"0000-0001-6165-5738"},{"first_name":"Skylar","last_name":"Gabel Eissens","full_name":"Gabel Eissens, Skylar"},{"first_name":"Miranda","last_name":"Gillitzer","full_name":"Gillitzer, Miranda"},{"first_name":"David","last_name":"Lippner","full_name":"Lippner, David"},{"last_name":"Disilvio","full_name":"Disilvio, Frank","first_name":"Frank"},{"first_name":"Casey","full_name":"Mueller, Casey","last_name":"Mueller"},{"last_name":"Wantuch","full_name":"Wantuch, Paeton","first_name":"Paeton"},{"full_name":"Chaffee, Gary","last_name":"Chaffee","first_name":"Gary"},{"last_name":"Famiglietti","full_name":"Famiglietti, Michael","first_name":"Michael"},{"first_name":"Danielle","full_name":"Zgoba, Danielle","last_name":"Zgoba"},{"first_name":"Asha","full_name":"Bailey, Asha","last_name":"Bailey"},{"first_name":"Yaya","full_name":"Bah, Yaya","last_name":"Bah"},{"first_name":"Samantha","full_name":"Engebretson, Samantha","last_name":"Engebretson"},{"first_name":"David","last_name":"Graupner","full_name":"Graupner, David"},{"first_name":"Emily","last_name":"Lackner","full_name":"Lackner, Emily"},{"last_name":"Larosa","full_name":"Larosa, Vincent","first_name":"Vincent"},{"first_name":"Tysha","last_name":"Medeiros","full_name":"Medeiros, Tysha"},{"full_name":"Olson, Michael","last_name":"Olson","first_name":"Michael"},{"last_name":"Phillips","full_name":"Phillips, Andrew","first_name":"Andrew"},{"first_name":"Harley","full_name":"Pyles, Harley","last_name":"Pyles"},{"last_name":"Richard","full_name":"Richard, Amanda","first_name":"Amanda"},{"first_name":"Scott","last_name":"Schoeller","full_name":"Schoeller, Scott"},{"first_name":"Boris","full_name":"Touzeau, Boris","last_name":"Touzeau"},{"last_name":"Williams","full_name":"Williams, Larry","first_name":"Larry"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"},{"last_name":"Peterson","full_name":"Peterson, Francis","first_name":"Francis"}],"external_id":{"pmid":["26115234"]},"article_processing_charge":"No","title":"Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites","publisher":"American Chemical Society","quality_controlled":"1","oa":1,"year":"2015","day":"26","publication":"Biochemistry","page":"4163 - 4166","doi":"10.1021/acs.biochem.5b00560","date_published":"2015-06-26T00:00:00Z","date_created":"2018-12-11T11:53:03Z"},{"project":[{"call_identifier":"FWF","_id":"2529486C-B435-11E9-9278-68D0E5697425","grant_number":"T 560-B17","name":"Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation"},{"name":"Cell Cortex and Germ Layer Formation in Zebrafish Gastrulation","grant_number":"I 812-B12","_id":"2527D5CC-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"Ruprecht, Verena, et al. “Cortical Contractility Triggers a Stochastic Switch to Fast Amoeboid Cell Motility.” Cell, vol. 160, no. 4, Cell Press, 2015, pp. 673–85, doi:10.1016/j.cell.2015.01.008.","ama":"Ruprecht V, Wieser S, Callan Jones A, et al. Cortical contractility triggers a stochastic switch to fast amoeboid cell motility. Cell. 2015;160(4):673-685. doi:10.1016/j.cell.2015.01.008","apa":"Ruprecht, V., Wieser, S., Callan Jones, A., Smutny, M., Morita, H., Sako, K., … Heisenberg, C.-P. J. (2015). Cortical contractility triggers a stochastic switch to fast amoeboid cell motility. Cell. Cell Press. https://doi.org/10.1016/j.cell.2015.01.008","ieee":"V. Ruprecht et al., “Cortical contractility triggers a stochastic switch to fast amoeboid cell motility,” Cell, vol. 160, no. 4. Cell Press, pp. 673–685, 2015.","short":"V. Ruprecht, S. Wieser, A. Callan Jones, M. Smutny, H. Morita, K. Sako, V. Barone, M. Ritsch Marte, M.K. Sixt, R. Voituriez, C.-P.J. Heisenberg, Cell 160 (2015) 673–685.","chicago":"Ruprecht, Verena, Stefan Wieser, Andrew Callan Jones, Michael Smutny, Hitoshi Morita, Keisuke Sako, Vanessa Barone, et al. “Cortical Contractility Triggers a Stochastic Switch to Fast Amoeboid Cell Motility.” Cell. Cell Press, 2015. https://doi.org/10.1016/j.cell.2015.01.008.","ista":"Ruprecht V, Wieser S, Callan Jones A, Smutny M, Morita H, Sako K, Barone V, Ritsch Marte M, Sixt MK, Voituriez R, Heisenberg C-PJ. 2015. Cortical contractility triggers a stochastic switch to fast amoeboid cell motility. Cell. 160(4), 673–685."},"title":"Cortical contractility triggers a stochastic switch to fast amoeboid cell motility","publist_id":"5634","author":[{"last_name":"Ruprecht","full_name":"Ruprecht, Verena","orcid":"0000-0003-4088-8633","id":"4D71A03A-F248-11E8-B48F-1D18A9856A87","first_name":"Verena"},{"id":"355AA5A0-F248-11E8-B48F-1D18A9856A87","first_name":"Stefan","last_name":"Wieser","full_name":"Wieser, Stefan","orcid":"0000-0002-2670-2217"},{"first_name":"Andrew","last_name":"Callan Jones","full_name":"Callan Jones, Andrew"},{"last_name":"Smutny","full_name":"Smutny, Michael","orcid":"0000-0002-5920-9090","first_name":"Michael","id":"3FE6E4E8-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Morita, Hitoshi","last_name":"Morita","first_name":"Hitoshi","id":"4C6E54C6-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Sako, Keisuke","orcid":"0000-0002-6453-8075","last_name":"Sako","id":"3BED66BE-F248-11E8-B48F-1D18A9856A87","first_name":"Keisuke"},{"last_name":"Barone","full_name":"Barone, Vanessa","orcid":"0000-0003-2676-3367","id":"419EECCC-F248-11E8-B48F-1D18A9856A87","first_name":"Vanessa"},{"first_name":"Monika","full_name":"Ritsch Marte, Monika","last_name":"Ritsch Marte"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"},{"full_name":"Voituriez, Raphaël","last_name":"Voituriez","first_name":"Raphaël"},{"first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","last_name":"Heisenberg","orcid":"0000-0002-0912-4566","full_name":"Heisenberg, Carl-Philipp J"}],"acknowledgement":"We would like to thank R. Hausschild and E. Papusheva for technical assistance and the service facilities at the IST Austria for continuous support. The caRhoA plasmid was a kind gift of T. Kudoh and A. Takesono. We thank M. Piel and E. Paluch for exchanging unpublished data. ","quality_controlled":"1","publisher":"Cell Press","oa":1,"day":"12","publication":"Cell","has_accepted_license":"1","year":"2015","doi":"10.1016/j.cell.2015.01.008","date_published":"2015-02-12T00:00:00Z","date_created":"2018-12-11T11:52:35Z","page":"673 - 685","_id":"1537","status":"public","pubrep_id":"484","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"ddc":["570"],"date_updated":"2023-09-07T12:05:08Z","file_date_updated":"2020-07-14T12:45:01Z","department":[{"_id":"CaHe"},{"_id":"MiSi"}],"oa_version":"Published Version","acknowledged_ssus":[{"_id":"SSU"}],"abstract":[{"lang":"eng","text":"3D amoeboid cell migration is central to many developmental and disease-related processes such as cancer metastasis. Here, we identify a unique prototypic amoeboid cell migration mode in early zebrafish embryos, termed stable-bleb migration. Stable-bleb cells display an invariant polarized balloon-like shape with exceptional migration speed and persistence. Progenitor cells can be reversibly transformed into stable-bleb cells irrespective of their primary fate and motile characteristics by increasing myosin II activity through biochemical or mechanical stimuli. Using a combination of theory and experiments, we show that, in stable-bleb cells, cortical contractility fluctuations trigger a stochastic switch into amoeboid motility, and a positive feedback between cortical flows and gradients in contractility maintains stable-bleb cell polarization. We further show that rearward cortical flows drive stable-bleb cell migration in various adhesive and non-adhesive environments, unraveling a highly versatile amoeboid migration phenotype."}],"month":"02","intvolume":" 160","scopus_import":1,"file":[{"creator":"system","date_updated":"2020-07-14T12:45:01Z","file_size":4362653,"date_created":"2018-12-12T10:13:21Z","file_name":"IST-2016-484-v1+1_1-s2.0-S0092867415000094-main.pdf","access_level":"open_access","relation":"main_file","content_type":"application/pdf","checksum":"228d3edf40627d897b3875088a0ac51f","file_id":"5003"}],"language":[{"iso":"eng"}],"publication_status":"published","related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"961"}]},"issue":"4","volume":160},{"abstract":[{"lang":"eng","text":"During inflammation, lymph nodes swell with an influx of immune cells. New findings identify a signalling pathway that induces relaxation in the contractile cells that give structure to these organs."}],"oa_version":"None","publisher":"Springer Nature","quality_controlled":"1","scopus_import":1,"month":"10","intvolume":" 514","year":"2014","publication_status":"published","day":"23","language":[{"iso":"eng"}],"publication":"Nature","page":"441 - 442","volume":514,"issue":"7523","date_published":"2014-10-23T00:00:00Z","doi":"10.1038/514441a","date_created":"2018-12-11T11:54:30Z","_id":"1877","type":"journal_article","article_type":"letter_note","status":"public","date_updated":"2021-01-12T06:53:47Z","citation":{"ista":"Sixt MK, Vaahtomeri K. 2014. Physiology: Relax and come in. Nature. 514(7523), 441–442.","chicago":"Sixt, Michael K, and Kari Vaahtomeri. “Physiology: Relax and Come In.” Nature. Springer Nature, 2014. https://doi.org/10.1038/514441a.","short":"M.K. Sixt, K. Vaahtomeri, Nature 514 (2014) 441–442.","ieee":"M. K. Sixt and K. Vaahtomeri, “Physiology: Relax and come in,” Nature, vol. 514, no. 7523. Springer Nature, pp. 441–442, 2014.","ama":"Sixt MK, Vaahtomeri K. Physiology: Relax and come in. Nature. 2014;514(7523):441-442. doi:10.1038/514441a","apa":"Sixt, M. K., & Vaahtomeri, K. (2014). Physiology: Relax and come in. Nature. Springer Nature. https://doi.org/10.1038/514441a","mla":"Sixt, Michael K., and Kari Vaahtomeri. “Physiology: Relax and Come In.” Nature, vol. 514, no. 7523, Springer Nature, 2014, pp. 441–42, doi:10.1038/514441a."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publist_id":"5219","author":[{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179"},{"id":"368EE576-F248-11E8-B48F-1D18A9856A87","first_name":"Kari","full_name":"Vaahtomeri, Kari","orcid":"0000-0001-7829-3518","last_name":"Vaahtomeri"}],"department":[{"_id":"MiSi"}],"title":"Physiology: Relax and come in"},{"date_created":"2018-12-11T11:54:40Z","doi":"10.1002/eji.201343681","date_published":"2014-02-01T00:00:00Z","issue":"2","volume":44,"page":"553 - 560","language":[{"iso":"eng"}],"publication":"European Journal of Immunology","day":"01","publication_status":"published","year":"2014","intvolume":" 44","month":"02","scopus_import":1,"publisher":"Wiley-Blackwell","acknowledgement":"FWF. Grant Number: P22058-B20","oa_version":"None","abstract":[{"text":"angerhans cells (LCs) are a unique subset of dendritic cells (DCs) that express epithelial adhesion molecules, allowing them to form contacts with epithelial cells and reside in epidermal/epithelial tissues. The dynamic regulation of epithelial adhesion plays a decisive role in the life cycle of LCs. It controls whether LCs remain immature and sessile within the epidermis or mature and egress to initiate immune responses. So far, the molecular machinery regulating epithelial adhesion molecules during LC maturation remains elusive. Here, we generated pure populations of immature human LCs in vitro to systematically probe for gene-expression changes during LC maturation. LCs down-regulate a set of epithelial genes including E-cadherin, while they upregulate the mesenchymal marker N-cadherin known to facilitate cell migration. In addition, N-cadherin is constitutively expressed by monocyte-derived DCs known to exhibit characteristics of both inflammatory-type and interstitial/dermal DCs. Moreover, the transcription factors ZEB1 and ZEB2 (ZEB is zinc-finger E-box-binding homeobox) are upregulated in migratory LCs. ZEB1 and ZEB2 have been shown to induce epithelial-to-mesenchymal transition (EMT) and invasive behavior in cancer cells undergoing metastasis. Our results provide the first hint that the molecular EMT machinery might facilitate LC mobilization. Moreover, our study suggests that N-cadherin plays a role during DC migration.","lang":"eng"}],"title":"Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2","department":[{"_id":"MiSi"}],"publist_id":"5185","author":[{"last_name":"Konradi","full_name":"Konradi, Sabine","first_name":"Sabine"},{"last_name":"Yasmin","full_name":"Yasmin, Nighat","first_name":"Nighat"},{"last_name":"Haslwanter","full_name":"Haslwanter, Denise","first_name":"Denise"},{"id":"3A3FC708-F248-11E8-B48F-1D18A9856A87","first_name":"Michele","last_name":"Weber","full_name":"Weber, Michele"},{"last_name":"Gesslbauer","full_name":"Gesslbauer, Bernd","first_name":"Bernd"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"},{"first_name":"Herbert","last_name":"Strobl","full_name":"Strobl, Herbert"}],"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","date_updated":"2021-01-12T06:54:01Z","citation":{"ieee":"S. Konradi et al., “Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2,” European Journal of Immunology, vol. 44, no. 2. Wiley-Blackwell, pp. 553–560, 2014.","short":"S. Konradi, N. Yasmin, D. Haslwanter, M. Weber, B. Gesslbauer, M.K. Sixt, H. Strobl, European Journal of Immunology 44 (2014) 553–560.","apa":"Konradi, S., Yasmin, N., Haslwanter, D., Weber, M., Gesslbauer, B., Sixt, M. K., & Strobl, H. (2014). Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2. European Journal of Immunology. Wiley-Blackwell. https://doi.org/10.1002/eji.201343681","ama":"Konradi S, Yasmin N, Haslwanter D, et al. Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2. European Journal of Immunology. 2014;44(2):553-560. doi:10.1002/eji.201343681","mla":"Konradi, Sabine, et al. “Langerhans Cell Maturation Is Accompanied by Induction of N-Cadherin and the Transcriptional Regulators of Epithelial-Mesenchymal Transition ZEB1/2.” European Journal of Immunology, vol. 44, no. 2, Wiley-Blackwell, 2014, pp. 553–60, doi:10.1002/eji.201343681.","ista":"Konradi S, Yasmin N, Haslwanter D, Weber M, Gesslbauer B, Sixt MK, Strobl H. 2014. Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2. European Journal of Immunology. 44(2), 553–560.","chicago":"Konradi, Sabine, Nighat Yasmin, Denise Haslwanter, Michele Weber, Bernd Gesslbauer, Michael K Sixt, and Herbert Strobl. “Langerhans Cell Maturation Is Accompanied by Induction of N-Cadherin and the Transcriptional Regulators of Epithelial-Mesenchymal Transition ZEB1/2.” European Journal of Immunology. Wiley-Blackwell, 2014. https://doi.org/10.1002/eji.201343681."},"status":"public","type":"journal_article","_id":"1910"},{"article_number":"125704","article_processing_charge":"No","publist_id":"5169","author":[{"first_name":"Constanze","last_name":"Lamprecht","full_name":"Lamprecht, Constanze"},{"first_name":"Birgit","last_name":"Plochberger","full_name":"Plochberger, Birgit"},{"orcid":"0000-0003-4088-8633","full_name":"Ruprecht, Verena","last_name":"Ruprecht","id":"4D71A03A-F248-11E8-B48F-1D18A9856A87","first_name":"Verena"},{"id":"355AA5A0-F248-11E8-B48F-1D18A9856A87","first_name":"Stefan","last_name":"Wieser","full_name":"Wieser, Stefan","orcid":"0000-0002-2670-2217"},{"full_name":"Rankl, Christian","last_name":"Rankl","first_name":"Christian"},{"first_name":"Elena","full_name":"Heister, Elena","last_name":"Heister"},{"last_name":"Unterauer","full_name":"Unterauer, Barbara","first_name":"Barbara"},{"first_name":"Mario","last_name":"Brameshuber","full_name":"Brameshuber, Mario"},{"full_name":"Danzberger, Jürgen","last_name":"Danzberger","first_name":"Jürgen"},{"full_name":"Lukanov, Petar","last_name":"Lukanov","first_name":"Petar"},{"last_name":"Flahaut","full_name":"Flahaut, Emmanuel","first_name":"Emmanuel"},{"last_name":"Schütz","full_name":"Schütz, Gerhard","first_name":"Gerhard"},{"first_name":"Peter","last_name":"Hinterdorfer","full_name":"Hinterdorfer, Peter"},{"first_name":"Andreas","full_name":"Ebner, Andreas","last_name":"Ebner"}],"title":"A single-molecule approach to explore binding uptake and transport of cancer cell targeting nanotubes","citation":{"ama":"Lamprecht C, Plochberger B, Ruprecht V, et al. A single-molecule approach to explore binding uptake and transport of cancer cell targeting nanotubes. Nanotechnology. 2014;25(12). doi:10.1088/0957-4484/25/12/125704","apa":"Lamprecht, C., Plochberger, B., Ruprecht, V., Wieser, S., Rankl, C., Heister, E., … Ebner, A. (2014). A single-molecule approach to explore binding uptake and transport of cancer cell targeting nanotubes. Nanotechnology. IOP Publishing. https://doi.org/10.1088/0957-4484/25/12/125704","short":"C. Lamprecht, B. Plochberger, V. Ruprecht, S. Wieser, C. Rankl, E. Heister, B. Unterauer, M. Brameshuber, J. Danzberger, P. Lukanov, E. Flahaut, G. Schütz, P. Hinterdorfer, A. Ebner, Nanotechnology 25 (2014).","ieee":"C. Lamprecht et al., “A single-molecule approach to explore binding uptake and transport of cancer cell targeting nanotubes,” Nanotechnology, vol. 25, no. 12. IOP Publishing, 2014.","mla":"Lamprecht, Constanze, et al. “A Single-Molecule Approach to Explore Binding Uptake and Transport of Cancer Cell Targeting Nanotubes.” Nanotechnology, vol. 25, no. 12, 125704, IOP Publishing, 2014, doi:10.1088/0957-4484/25/12/125704.","ista":"Lamprecht C, Plochberger B, Ruprecht V, Wieser S, Rankl C, Heister E, Unterauer B, Brameshuber M, Danzberger J, Lukanov P, Flahaut E, Schütz G, Hinterdorfer P, Ebner A. 2014. A single-molecule approach to explore binding uptake and transport of cancer cell targeting nanotubes. Nanotechnology. 25(12), 125704.","chicago":"Lamprecht, Constanze, Birgit Plochberger, Verena Ruprecht, Stefan Wieser, Christian Rankl, Elena Heister, Barbara Unterauer, et al. “A Single-Molecule Approach to Explore Binding Uptake and Transport of Cancer Cell Targeting Nanotubes.” Nanotechnology. IOP Publishing, 2014. https://doi.org/10.1088/0957-4484/25/12/125704."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","oa":1,"publisher":"IOP Publishing","acknowledgement":"This work was supported by EC grant Marie Curie RTN-CT-2006-035616, CARBIO 'Carbon nanotubes for biomedical applications' and Austrian FFG grant mnt-era.net 823980, 'IntelliTip'.\r\n","date_created":"2018-12-11T11:54:45Z","date_published":"2014-03-28T00:00:00Z","doi":"10.1088/0957-4484/25/12/125704","year":"2014","has_accepted_license":"1","publication":"Nanotechnology","day":"28","article_type":"original","type":"journal_article","status":"public","_id":"1925","department":[{"_id":"CaHe"},{"_id":"MiSi"}],"file_date_updated":"2020-07-14T12:45:21Z","date_updated":"2021-01-12T06:54:07Z","ddc":["570"],"scopus_import":1,"intvolume":" 25","month":"03","abstract":[{"text":"In the past decade carbon nanotubes (CNTs) have been widely studied as a potential drug-delivery system, especially with functionality for cellular targeting. Yet, little is known about the actual process of docking to cell receptors and transport dynamics after internalization. Here we performed single-particle studies of folic acid (FA) mediated CNT binding to human carcinoma cells and their transport inside the cytosol. In particular, we employed molecular recognition force spectroscopy, an atomic force microscopy based method, to visualize and quantify docking of FA functionalized CNTs to FA binding receptors in terms of binding probability and binding force. We then traced individual fluorescently labeled, FA functionalized CNTs after specific uptake, and created a dynamic 'roadmap' that clearly showed trajectories of directed diffusion and areas of nanotube confinement in the cytosol. Our results demonstrate the potential of a single-molecule approach for investigation of drug-delivery vehicles and their targeting capacity.","lang":"eng"}],"oa_version":"Submitted Version","volume":25,"issue":"12","publication_status":"published","language":[{"iso":"eng"}],"file":[{"file_id":"7856","checksum":"df4e03d225a19179e7790f6d87a12332","access_level":"open_access","relation":"main_file","content_type":"application/pdf","date_created":"2020-05-15T09:21:19Z","file_name":"2014_Nanotechnology_Lamprecht.pdf","creator":"dernst","date_updated":"2020-07-14T12:45:21Z","file_size":3804152}]},{"volume":30,"issue":"1","language":[{"iso":"eng"}],"publication_status":"published","intvolume":" 30","month":"10","main_file_link":[{"url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4177954/","open_access":"1"}],"scopus_import":1,"oa_version":"Submitted Version","pmid":1,"abstract":[{"text":"Directional guidance of migrating cells is relatively well explored in the reductionist setting of cell culture experiments. Here spatial gradients of chemical cues as well as gradients of mechanical substrate characteristics prove sufficient to attract single cells as well as their collectives. How such gradients present and act in the context of an organism is far less clear. Here we review recent advances in understanding how guidance cues emerge and operate in the physiological context.","lang":"eng"}],"department":[{"_id":"MiSi"}],"date_updated":"2021-01-12T06:55:40Z","status":"public","type":"journal_article","_id":"2158","date_created":"2018-12-11T11:56:03Z","doi":"10.1016/j.ceb.2014.05.010","date_published":"2014-10-01T00:00:00Z","page":"33 - 40","publication":"Current Opinion in Cell Biology","day":"01","year":"2014","oa":1,"quality_controlled":"1","publisher":"Elsevier","acknowledgement":"This effort was supported by the Intramural Research Program of the Center for Cancer Research, NCI, National Institutes of Health and the European Research Council (ERC).","title":"New paradigms in the establishment and maintenance of gradients during directed cell migration","external_id":{"pmid":["24959970"]},"publist_id":"4848","author":[{"first_name":"Ritankar","full_name":"Majumdar, Ritankar","last_name":"Majumdar"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"},{"full_name":"Parent, Carole","last_name":"Parent","first_name":"Carole"}],"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","citation":{"ieee":"R. Majumdar, M. K. Sixt, and C. Parent, “New paradigms in the establishment and maintenance of gradients during directed cell migration,” Current Opinion in Cell Biology, vol. 30, no. 1. Elsevier, pp. 33–40, 2014.","short":"R. Majumdar, M.K. Sixt, C. Parent, Current Opinion in Cell Biology 30 (2014) 33–40.","ama":"Majumdar R, Sixt MK, Parent C. New paradigms in the establishment and maintenance of gradients during directed cell migration. Current Opinion in Cell Biology. 2014;30(1):33-40. doi:10.1016/j.ceb.2014.05.010","apa":"Majumdar, R., Sixt, M. K., & Parent, C. (2014). New paradigms in the establishment and maintenance of gradients during directed cell migration. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2014.05.010","mla":"Majumdar, Ritankar, et al. “New Paradigms in the Establishment and Maintenance of Gradients during Directed Cell Migration.” Current Opinion in Cell Biology, vol. 30, no. 1, Elsevier, 2014, pp. 33–40, doi:10.1016/j.ceb.2014.05.010.","ista":"Majumdar R, Sixt MK, Parent C. 2014. New paradigms in the establishment and maintenance of gradients during directed cell migration. Current Opinion in Cell Biology. 30(1), 33–40.","chicago":"Majumdar, Ritankar, Michael K Sixt, and Carole Parent. “New Paradigms in the Establishment and Maintenance of Gradients during Directed Cell Migration.” Current Opinion in Cell Biology. Elsevier, 2014. https://doi.org/10.1016/j.ceb.2014.05.010."}},{"publication":"PLoS One","day":"22","year":"2014","has_accepted_license":"1","date_created":"2018-12-11T11:56:22Z","doi":"10.1371/journal.pone.0085699","date_published":"2014-01-22T00:00:00Z","acknowledgement":"Michael Sixt's research is supported by the European Research Council (ERC Starting grant).","oa":1,"publisher":"Public Library of Science","quality_controlled":"1","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","citation":{"ista":"Stoler Barak L, Moussion C, Shezen E, Hatzav M, Sixt MK, Alon R. 2014. Blood vessels pattern heparan sulfate gradients between their apical and basolateral aspects. PLoS One. 9(1), e85699.","chicago":"Stoler Barak, Liat, Christine Moussion, Elias Shezen, Miki Hatzav, Michael K Sixt, and Ronen Alon. “Blood Vessels Pattern Heparan Sulfate Gradients between Their Apical and Basolateral Aspects.” PLoS One. Public Library of Science, 2014. https://doi.org/10.1371/journal.pone.0085699.","ieee":"L. Stoler Barak, C. Moussion, E. Shezen, M. Hatzav, M. K. Sixt, and R. Alon, “Blood vessels pattern heparan sulfate gradients between their apical and basolateral aspects,” PLoS One, vol. 9, no. 1. Public Library of Science, 2014.","short":"L. Stoler Barak, C. Moussion, E. Shezen, M. Hatzav, M.K. Sixt, R. Alon, PLoS One 9 (2014).","ama":"Stoler Barak L, Moussion C, Shezen E, Hatzav M, Sixt MK, Alon R. Blood vessels pattern heparan sulfate gradients between their apical and basolateral aspects. PLoS One. 2014;9(1). doi:10.1371/journal.pone.0085699","apa":"Stoler Barak, L., Moussion, C., Shezen, E., Hatzav, M., Sixt, M. K., & Alon, R. (2014). Blood vessels pattern heparan sulfate gradients between their apical and basolateral aspects. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0085699","mla":"Stoler Barak, Liat, et al. “Blood Vessels Pattern Heparan Sulfate Gradients between Their Apical and Basolateral Aspects.” PLoS One, vol. 9, no. 1, e85699, Public Library of Science, 2014, doi:10.1371/journal.pone.0085699."},"title":"Blood vessels pattern heparan sulfate gradients between their apical and basolateral aspects","author":[{"first_name":"Liat","full_name":"Stoler Barak, Liat","last_name":"Stoler Barak"},{"full_name":"Moussion, Christine","last_name":"Moussion","first_name":"Christine","id":"3356F664-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Shezen","full_name":"Shezen, Elias","first_name":"Elias"},{"first_name":"Miki","last_name":"Hatzav","full_name":"Hatzav, Miki"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"},{"first_name":"Ronen","last_name":"Alon","full_name":"Alon, Ronen"}],"publist_id":"4756","article_number":"e85699","project":[{"grant_number":"289720","name":"Stromal Cell-immune Cell Interactions in Health and Disease","call_identifier":"FP7","_id":"25A76F58-B435-11E9-9278-68D0E5697425"}],"language":[{"iso":"eng"}],"file":[{"creator":"system","file_size":12634775,"date_updated":"2020-07-14T12:45:33Z","file_name":"IST-2016-433-v1+1_journal.pone.0085699.pdf","date_created":"2018-12-12T10:07:48Z","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_id":"4646","checksum":"84a8033bda2e07e39405f5acc85f4eca"}],"publication_status":"published","ec_funded":1,"volume":9,"issue":"1","oa_version":"Published Version","abstract":[{"lang":"eng","text":"A hallmark of immune cell trafficking is directional guidance via gradients of soluble or surface bound chemokines. Vascular endothelial cells produce, transport and deposit either their own chemokines or chemokines produced by the underlying stroma. Endothelial heparan sulfate (HS) was suggested to be a critical scaffold for these chemokine pools, but it is unclear how steep chemokine gradients are sustained between the lumenal and ablumenal aspects of blood vessels. Addressing this question by semi-quantitative immunostaining of HS moieties around blood vessels with a pan anti-HS IgM mAb, we found a striking HS enrichment in the basal lamina of resting and inflamed post capillary skin venules, as well as in high endothelial venules (HEVs) of lymph nodes. Staining of skin vessels with a glycocalyx probe further suggested that their lumenal glycocalyx contains much lower HS density than their basolateral extracellular matrix (ECM). This polarized HS pattern was observed also in isolated resting and inflamed microvascular dermal cells. Notably, progressive skin inflammation resulted in massive ECM deposition and in further HS enrichment around skin post capillary venules and their associated pericytes. Inflammation-dependent HS enrichment was not compromised in mice deficient in the main HS degrading enzyme, heparanase. Our results suggest that the blood vasculature patterns steep gradients of HS scaffolds between their lumenal and basolateral endothelial aspects, and that inflammatory processes can further enrich the HS content nearby inflamed vessels. We propose that chemokine gradients between the lumenal and ablumenal sides of vessels could be favored by these sharp HS scaffold gradients."}],"intvolume":" 9","month":"01","scopus_import":1,"ddc":["570"],"date_updated":"2021-01-12T06:56:03Z","file_date_updated":"2020-07-14T12:45:33Z","department":[{"_id":"MiSi"}],"_id":"2214","pubrep_id":"433","status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article"},{"day":"14","publication":"Nature Reviews Molecular Cell Biology","language":[{"iso":"eng"}],"publication_status":"published","year":"2014","issue":"6","volume":15,"doi":"10.1038/nrm3805","date_published":"2014-05-14T00:00:00Z","date_created":"2018-12-11T11:56:22Z","page":"369 - 383","oa_version":"None","acknowledgement":"J.R. was supported by a Boehringer Ingelheim Fonds PhD stipend.","abstract":[{"lang":"eng","text":"Homologous recombination is crucial for genome stability and for genetic exchange. Although our knowledge of the principle steps in recombination and its machinery is well advanced, homology search, the critical step of exploring the genome for homologous sequences to enable recombination, has remained mostly enigmatic. However, recent methodological advances have provided considerable new insights into this fundamental step in recombination that can be integrated into a mechanistic model. These advances emphasize the importance of genomic proximity and nuclear organization for homology search and the critical role of homology search mediators in this process. They also aid our understanding of how homology search might lead to unwanted and potentially disease-promoting recombination events."}],"month":"05","intvolume":" 15","scopus_import":1,"quality_controlled":"1","publisher":"Nature Publishing Group","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","citation":{"ama":"Renkawitz J, Lademann C, Jentsch S. Mechanisms and principles of homology search during recombination. Nature Reviews Molecular Cell Biology. 2014;15(6):369-383. doi:10.1038/nrm3805","apa":"Renkawitz, J., Lademann, C., & Jentsch, S. (2014). Mechanisms and principles of homology search during recombination. Nature Reviews Molecular Cell Biology. Nature Publishing Group. https://doi.org/10.1038/nrm3805","short":"J. Renkawitz, C. Lademann, S. Jentsch, Nature Reviews Molecular Cell Biology 15 (2014) 369–383.","ieee":"J. Renkawitz, C. Lademann, and S. Jentsch, “Mechanisms and principles of homology search during recombination,” Nature Reviews Molecular Cell Biology, vol. 15, no. 6. Nature Publishing Group, pp. 369–383, 2014.","mla":"Renkawitz, Jörg, et al. “Mechanisms and Principles of Homology Search during Recombination.” Nature Reviews Molecular Cell Biology, vol. 15, no. 6, Nature Publishing Group, 2014, pp. 369–83, doi:10.1038/nrm3805.","ista":"Renkawitz J, Lademann C, Jentsch S. 2014. Mechanisms and principles of homology search during recombination. Nature Reviews Molecular Cell Biology. 15(6), 369–383.","chicago":"Renkawitz, Jörg, Claudio Lademann, and Stefan Jentsch. “Mechanisms and Principles of Homology Search during Recombination.” Nature Reviews Molecular Cell Biology. Nature Publishing Group, 2014. https://doi.org/10.1038/nrm3805."},"date_updated":"2021-01-12T06:56:03Z","title":"Mechanisms and principles of homology search during recombination","department":[{"_id":"MiSi"}],"author":[{"id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","first_name":"Jörg","last_name":"Renkawitz","orcid":"0000-0003-2856-3369","full_name":"Renkawitz, Jörg"},{"first_name":"Claudio","full_name":"Lademann, Claudio","last_name":"Lademann"},{"full_name":"Jentsch, Stefan","last_name":"Jentsch","first_name":"Stefan"}],"publist_id":"4755","_id":"2215","status":"public","type":"journal_article"},{"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","citation":{"ieee":"A. Dueck, A. Eichner, M. K. Sixt, and G. Meister, “A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation,” FEBS Letters, vol. 588, no. 4. Elsevier, pp. 632–640, 2014.","short":"A. Dueck, A. Eichner, M.K. Sixt, G. Meister, FEBS Letters 588 (2014) 632–640.","apa":"Dueck, A., Eichner, A., Sixt, M. K., & Meister, G. (2014). A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation. FEBS Letters. Elsevier. https://doi.org/10.1016/j.febslet.2014.01.009","ama":"Dueck A, Eichner A, Sixt MK, Meister G. A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation. FEBS Letters. 2014;588(4):632-640. doi:10.1016/j.febslet.2014.01.009","mla":"Dueck, Anne, et al. “A MiR-155-Dependent MicroRNA Hierarchy in Dendritic Cell Maturation and Macrophage Activation.” FEBS Letters, vol. 588, no. 4, Elsevier, 2014, pp. 632–40, doi:10.1016/j.febslet.2014.01.009.","ista":"Dueck A, Eichner A, Sixt MK, Meister G. 2014. A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation. FEBS Letters. 588(4), 632–640.","chicago":"Dueck, Anne, Alexander Eichner, Michael K Sixt, and Gunter Meister. “A MiR-155-Dependent MicroRNA Hierarchy in Dendritic Cell Maturation and Macrophage Activation.” FEBS Letters. Elsevier, 2014. https://doi.org/10.1016/j.febslet.2014.01.009."},"date_updated":"2021-01-12T06:56:14Z","title":"A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation","department":[{"_id":"MiSi"}],"publist_id":"4714","author":[{"last_name":"Dueck","full_name":"Dueck, Anne","first_name":"Anne"},{"full_name":"Eichner, Alexander","last_name":"Eichner","first_name":"Alexander","id":"4DFA52AE-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"},{"first_name":"Gunter","last_name":"Meister","full_name":"Meister, Gunter"}],"_id":"2242","status":"public","type":"journal_article","day":"14","publication":"FEBS Letters","language":[{"iso":"eng"}],"publication_identifier":{"issn":["00145793"]},"year":"2014","publication_status":"published","doi":"10.1016/j.febslet.2014.01.009","issue":"4","date_published":"2014-02-14T00:00:00Z","volume":588,"date_created":"2018-12-11T11:56:31Z","page":"632 - 640","oa_version":"None","abstract":[{"lang":"eng","text":"MicroRNAs (miRNAs) are small RNAs that play important regulatory roles in many cellular pathways. MiRNAs associate with members of the Argonaute protein family and bind to partially complementary sequences on mRNAs and induce translational repression or mRNA decay. Using deep sequencing and Northern blotting, we characterized miRNA expression in wild type and miR-155-deficient dendritic cells (DCs) and macrophages. Analysis of different stimuli (LPS, LDL, eLDL, oxLDL) reveals a direct influence of miR-155 on the expression levels of other miRNAs. For example, miR-455 is negatively regulated in miR-155-deficient cells possibly due to inhibition of the transcription factor C/EBPbeta by miR-155. Based on our comprehensive data sets, we propose a model of hierarchical miRNA expression dominated by miR-155 in DCs and macrophages."}],"month":"02","intvolume":" 588","publisher":"Elsevier","quality_controlled":"1","scopus_import":1},{"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2021-01-12T07:00:01Z","citation":{"mla":"Moussion, Christine, and Michael K. Sixt. “A Conduit to Amplify Innate Immunity.” Immunity, vol. 38, no. 5, Cell Press, 2013, pp. 853–54, doi:10.1016/j.immuni.2013.05.005.","apa":"Moussion, C., & Sixt, M. K. (2013). A conduit to amplify innate immunity. Immunity. Cell Press. https://doi.org/10.1016/j.immuni.2013.05.005","ama":"Moussion C, Sixt MK. A conduit to amplify innate immunity. Immunity. 2013;38(5):853-854. doi:10.1016/j.immuni.2013.05.005","short":"C. Moussion, M.K. Sixt, Immunity 38 (2013) 853–854.","ieee":"C. Moussion and M. K. Sixt, “A conduit to amplify innate immunity,” Immunity, vol. 38, no. 5. Cell Press, pp. 853–854, 2013.","chicago":"Moussion, Christine, and Michael K Sixt. “A Conduit to Amplify Innate Immunity.” Immunity. Cell Press, 2013. https://doi.org/10.1016/j.immuni.2013.05.005.","ista":"Moussion C, Sixt MK. 2013. A conduit to amplify innate immunity. Immunity. 38(5), 853–854."},"title":"A conduit to amplify innate immunity","department":[{"_id":"MiSi"}],"publist_id":"3969","author":[{"full_name":"Moussion, Christine","last_name":"Moussion","first_name":"Christine","id":"3356F664-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt"}],"_id":"2830","status":"public","type":"journal_article","day":"23","language":[{"iso":"eng"}],"publication":"Immunity","year":"2013","publication_status":"published","date_published":"2013-05-23T00:00:00Z","volume":38,"doi":"10.1016/j.immuni.2013.05.005","issue":"5","date_created":"2018-12-11T11:59:49Z","page":"853 - 854","oa_version":"None","month":"05","intvolume":" 38","scopus_import":1,"quality_controlled":"1","publisher":"Cell Press"}]