[{"publication_status":"published","department":[{"_id":"MiSi"},{"_id":"Bio"}],"publisher":"Cell Press","year":"2017","date_updated":"2023-09-28T11:33:49Z","date_created":"2018-12-11T11:48:10Z","volume":171,"author":[{"full_name":"Mueller, Jan","last_name":"Mueller","first_name":"Jan"},{"id":"4BFB7762-F248-11E8-B48F-1D18A9856A87","last_name":"Szep","first_name":"Gregory","full_name":"Szep, Gregory"},{"last_name":"Nemethova","first_name":"Maria","id":"34E27F1C-F248-11E8-B48F-1D18A9856A87","full_name":"Nemethova, Maria"},{"first_name":"Ingrid","last_name":"De Vries","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","full_name":"De Vries, Ingrid"},{"last_name":"Lieber","first_name":"Arnon","full_name":"Lieber, Arnon"},{"first_name":"Christoph","last_name":"Winkler","full_name":"Winkler, Christoph"},{"full_name":"Kruse, Karsten","last_name":"Kruse","first_name":"Karsten"},{"full_name":"Small, John","first_name":"John","last_name":"Small"},{"full_name":"Schmeiser, Christian","first_name":"Christian","last_name":"Schmeiser"},{"full_name":"Keren, Kinneret","last_name":"Keren","first_name":"Kinneret"},{"last_name":"Hauschild","first_name":"Robert","orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","full_name":"Hauschild, Robert"},{"last_name":"Sixt","first_name":"Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K"}],"ec_funded":1,"publist_id":"6951","isi":1,"quality_controlled":"1","project":[{"name":"Modeling of Polarization and Motility of Leukocytes in Three-Dimensional Environments","_id":"25AD6156-B435-11E9-9278-68D0E5697425","grant_number":"LS13-029"},{"grant_number":"281556","_id":"25A603A2-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","call_identifier":"FP7"}],"external_id":{"isi":["000411331800020"]},"acknowledged_ssus":[{"_id":"ScienComp"}],"language":[{"iso":"eng"}],"doi":"10.1016/j.cell.2017.07.051","month":"09","publication_identifier":{"issn":["00928674"]},"title":"Load adaptation of lamellipodial actin networks","status":"public","intvolume":" 171","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","_id":"727","oa_version":"None","type":"journal_article","abstract":[{"lang":"eng","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."}],"issue":"1","page":"188 - 200","publication":"Cell","citation":{"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.","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.","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.","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","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","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."},"date_published":"2017-09-21T00:00:00Z","scopus_import":"1","day":"21","article_processing_charge":"No"},{"date_created":"2018-12-12T12:31:34Z","date_updated":"2024-02-21T13:47:00Z","oa_version":"Published Version","file":[{"relation":"main_file","file_id":"5612","date_created":"2018-12-12T13:02:47Z","date_updated":"2020-07-14T12:47:04Z","checksum":"3d6942d47d0737d064706b5728c4d8c8","file_name":"IST-2017-71-v1+1_Synapse_1.avi","access_level":"open_access","file_size":236204020,"content_type":"video/x-msvideo","creator":"system"},{"file_name":"IST-2017-71-v1+2_Synapse_2.avi","access_level":"open_access","content_type":"video/x-msvideo","file_size":226232496,"creator":"system","relation":"main_file","file_id":"5613","date_updated":"2020-07-14T12:47:04Z","date_created":"2018-12-12T13:02:51Z","checksum":"4850006c047b0147a9e85b3c2f6f0af4"}],"author":[{"full_name":"Leithner, Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-1073-744X","first_name":"Alexander F","last_name":"Leithner"}],"status":"public","title":"Immunological synapse DC-Tcells","ddc":["570"],"department":[{"_id":"MiSi"}],"publisher":"Institute of Science and Technology Austria","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"5567","year":"2017","license":"https://creativecommons.org/publicdomain/zero/1.0/","abstract":[{"lang":"eng","text":"Immunological synapse DC-Tcells"}],"file_date_updated":"2020-07-14T12:47:04Z","datarep_id":"71","type":"research_data","doi":"10.15479/AT:ISTA:71","date_published":"2017-08-09T00:00:00Z","tmp":{"short":"CC0 (1.0)","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)"},"oa":1,"citation":{"chicago":"Leithner, Alexander F. “Immunological Synapse DC-Tcells.” Institute of Science and Technology Austria, 2017. https://doi.org/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.","short":"A.F. Leithner, (2017).","ista":"Leithner AF. 2017. Immunological synapse DC-Tcells, Institute of Science and Technology Austria, 10.15479/AT:ISTA:71.","ieee":"A. F. Leithner, “Immunological synapse DC-Tcells.” Institute of Science and Technology Austria, 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"},"day":"09","month":"08","article_processing_charge":"No","has_accepted_license":"1","keyword":["Immunological synapse"]},{"issue":"4","publist_id":"7065","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"}],"type":"journal_article","oa_version":"None","volume":46,"date_created":"2018-12-11T11:47:47Z","date_updated":"2024-03-28T23:30:09Z","related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"6947"}]},"author":[{"first_name":"Frank P","last_name":"Assen","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-3470-6119","full_name":"Assen, Frank P"},{"full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"intvolume":" 46","publisher":"Cell Press","department":[{"_id":"MiSi"}],"publication_status":"published","status":"public","title":"The dynamic cytokine niche","year":"2017","_id":"664","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"issn":["10747613"]},"month":"04","day":"18","scopus_import":1,"language":[{"iso":"eng"}],"date_published":"2017-04-18T00:00:00Z","doi":"10.1016/j.immuni.2017.04.006","page":"519 - 520","quality_controlled":"1","citation":{"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","ieee":"F. P. Assen and M. K. Sixt, “The dynamic cytokine niche,” Immunity, vol. 46, no. 4. Cell Press, pp. 519–520, 2017.","ista":"Assen FP, Sixt MK. 2017. The dynamic cytokine niche. Immunity. 46(4), 519–520.","short":"F.P. Assen, M.K. Sixt, Immunity 46 (2017) 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.","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."},"publication":"Immunity"},{"publication":"The Journal of Clinical Investigation","citation":{"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","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.","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.","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.","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.","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."},"page":"2051 - 2065","date_published":"2017-06-01T00:00:00Z","scopus_import":1,"day":"01","_id":"679","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection","status":"public","intvolume":" 127","oa_version":"Submitted Version","type":"journal_article","abstract":[{"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.","lang":"eng"}],"issue":"6","external_id":{"pmid":["28504646"]},"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5451238/","open_access":"1"}],"oa":1,"quality_controlled":"1","project":[{"_id":"25985A36-B435-11E9-9278-68D0E5697425","grant_number":"T00817-B21","name":"The biochemical basis of PAR polarization","call_identifier":"FWF"},{"call_identifier":"FWF","name":"Revealing the mechanisms underlying drug interactions","grant_number":"P27201-B22","_id":"25E9AF9E-B435-11E9-9278-68D0E5697425"}],"doi":"10.1172/JCI80631","language":[{"iso":"eng"}],"month":"06","publication_identifier":{"issn":["00219738"]},"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.","year":"2017","pmid":1,"publication_status":"published","publisher":"American Society for Clinical Investigation","department":[{"_id":"MiSi"}],"author":[{"last_name":"Ebner","first_name":"Florian","full_name":"Ebner, Florian"},{"full_name":"Sedlyarov, Vitaly","first_name":"Vitaly","last_name":"Sedlyarov"},{"first_name":"Saren","last_name":"Tasciyan","id":"4323B49C-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-1671-393X","full_name":"Tasciyan, Saren"},{"full_name":"Ivin, Masa","last_name":"Ivin","first_name":"Masa"},{"full_name":"Kratochvill, Franz","first_name":"Franz","last_name":"Kratochvill"},{"first_name":"Nina","last_name":"Gratz","full_name":"Gratz, Nina"},{"full_name":"Kenner, Lukas","first_name":"Lukas","last_name":"Kenner"},{"full_name":"Villunger, Andreas","first_name":"Andreas","last_name":"Villunger"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","first_name":"Michael K","last_name":"Sixt","full_name":"Sixt, Michael K"},{"full_name":"Kovarik, Pavel","last_name":"Kovarik","first_name":"Pavel"}],"related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"12401"}]},"date_updated":"2024-03-28T23:30:23Z","date_created":"2018-12-11T11:47:53Z","volume":127,"publist_id":"7038"},{"publication":"Nature Immunology","citation":{"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","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.","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.","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","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.","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.","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."},"article_type":"original","page":"1352 - 1360","date_published":"2016-12-01T00:00:00Z","scopus_import":1,"day":"01","article_processing_charge":"No","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"1137","title":"RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics","status":"public","intvolume":" 17","oa_version":"Submitted Version","type":"journal_article","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"}],"issue":"12","oa":1,"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6400263"}],"external_id":{"pmid":["27776107"]},"quality_controlled":"1","doi":"10.1038/ni.3575","language":[{"iso":"eng"}],"month":"12","year":"2016","pmid":1,"publication_status":"published","department":[{"_id":"MiSi"}],"publisher":"Nature Publishing Group","author":[{"full_name":"Salzer, Elisabeth","last_name":"Salzer","first_name":"Elisabeth"},{"last_name":"Çaǧdaş","first_name":"Deniz","full_name":"Çaǧdaş, Deniz"},{"id":"4167FE56-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6625-3348","first_name":"Miroslav","last_name":"Hons","full_name":"Hons, Miroslav"},{"full_name":"Mace, Emily","first_name":"Emily","last_name":"Mace"},{"full_name":"Garncarz, Wojciech","first_name":"Wojciech","last_name":"Garncarz"},{"first_name":"Oezlem","last_name":"Petronczki","full_name":"Petronczki, Oezlem"},{"full_name":"Platzer, René","last_name":"Platzer","first_name":"René"},{"full_name":"Pfajfer, Laurène","last_name":"Pfajfer","first_name":"Laurène"},{"full_name":"Bilic, Ivan","first_name":"Ivan","last_name":"Bilic"},{"first_name":"Sol","last_name":"Ban","full_name":"Ban, Sol"},{"first_name":"Katharina","last_name":"Willmann","full_name":"Willmann, Katharina"},{"full_name":"Mukherjee, Malini","first_name":"Malini","last_name":"Mukherjee"},{"full_name":"Supper, Verena","first_name":"Verena","last_name":"Supper"},{"full_name":"Hsu, Hsiangting","last_name":"Hsu","first_name":"Hsiangting"},{"last_name":"Banerjee","first_name":"Pinaki","full_name":"Banerjee, Pinaki"},{"last_name":"Sinha","first_name":"Papiya","full_name":"Sinha, Papiya"},{"full_name":"Mcclanahan, Fabienne","last_name":"Mcclanahan","first_name":"Fabienne"},{"last_name":"Zlabinger","first_name":"Gerhard","full_name":"Zlabinger, Gerhard"},{"first_name":"Winfried","last_name":"Pickl","full_name":"Pickl, Winfried"},{"first_name":"John","last_name":"Gribben","full_name":"Gribben, John"},{"last_name":"Stockinger","first_name":"Hannes","full_name":"Stockinger, Hannes"},{"last_name":"Bennett","first_name":"Keiryn","full_name":"Bennett, Keiryn"},{"first_name":"Johannes","last_name":"Huppa","full_name":"Huppa, Johannes"},{"first_name":"Loï̈C","last_name":"Dupré","full_name":"Dupré, Loï̈C"},{"first_name":"Özden","last_name":"Sanal","full_name":"Sanal, Özden"},{"full_name":"Jäger, Ulrich","last_name":"Jäger","first_name":"Ulrich"},{"full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Tezcan, Ilhan","last_name":"Tezcan","first_name":"Ilhan"},{"last_name":"Orange","first_name":"Jordan","full_name":"Orange, Jordan"},{"last_name":"Boztug","first_name":"Kaan","full_name":"Boztug, Kaan"}],"date_updated":"2021-01-12T06:48:33Z","date_created":"2018-12-11T11:50:21Z","volume":17,"publist_id":"6221"},{"month":"12","language":[{"iso":"eng"}],"doi":"10.1038/ni.3590","quality_controlled":"1","oa":1,"main_file_link":[{"open_access":"1","url":"https://ora.ox.ac.uk/objects/uuid:f53a464e-1e5b-4f08-a7d8-b6749b852b9d"}],"publist_id":"6216","volume":17,"date_updated":"2021-01-12T06:48:36Z","date_created":"2018-12-11T11:50:22Z","author":[{"full_name":"Martins, Rui","first_name":"Rui","last_name":"Martins"},{"first_name":"Julia","last_name":"Maier","full_name":"Maier, Julia"},{"full_name":"Gorki, Anna","first_name":"Anna","last_name":"Gorki"},{"last_name":"Huber","first_name":"Kilian","full_name":"Huber, Kilian"},{"first_name":"Omar","last_name":"Sharif","full_name":"Sharif, Omar"},{"last_name":"Starkl","first_name":"Philipp","full_name":"Starkl, Philipp"},{"last_name":"Saluzzo","first_name":"Simona","full_name":"Saluzzo, Simona"},{"last_name":"Quattrone","first_name":"Federica","full_name":"Quattrone, Federica"},{"full_name":"Gawish, Riem","first_name":"Riem","last_name":"Gawish"},{"full_name":"Lakovits, Karin","first_name":"Karin","last_name":"Lakovits"},{"full_name":"Aichinger, Michael","last_name":"Aichinger","first_name":"Michael"},{"last_name":"Radic Sarikas","first_name":"Branka","full_name":"Radic Sarikas, Branka"},{"full_name":"Lardeau, Charles","first_name":"Charles","last_name":"Lardeau"},{"last_name":"Hladik","first_name":"Anastasiya","full_name":"Hladik, Anastasiya"},{"full_name":"Korosec, Ana","first_name":"Ana","last_name":"Korosec"},{"id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","last_name":"Brown","first_name":"Markus","full_name":"Brown, Markus"},{"full_name":"Vaahtomeri, Kari","orcid":"0000-0001-7829-3518","id":"368EE576-F248-11E8-B48F-1D18A9856A87","last_name":"Vaahtomeri","first_name":"Kari"},{"last_name":"Duggan","first_name":"Michelle","id":"2EDEA62C-F248-11E8-B48F-1D18A9856A87","full_name":"Duggan, Michelle"},{"full_name":"Kerjaschki, Dontscho","last_name":"Kerjaschki","first_name":"Dontscho"},{"full_name":"Esterbauer, Harald","first_name":"Harald","last_name":"Esterbauer"},{"full_name":"Colinge, Jacques","last_name":"Colinge","first_name":"Jacques"},{"first_name":"Stephanie","last_name":"Eisenbarth","full_name":"Eisenbarth, Stephanie"},{"last_name":"Decker","first_name":"Thomas","full_name":"Decker, 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","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"},{"first_name":"Giulio","last_name":"Superti Furga","full_name":"Superti Furga, Giulio"},{"last_name":"Knapp","first_name":"Sylvia","full_name":"Knapp, Sylvia"}],"department":[{"_id":"MiSi"},{"_id":"PeJo"}],"publisher":"Nature Publishing Group","publication_status":"published","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).","year":"2016","day":"01","scopus_import":1,"date_published":"2016-12-01T00:00:00Z","page":"1361 - 1372","citation":{"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.","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.","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.","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.","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","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.","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"},"publication":"Nature Immunology","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."}],"type":"journal_article","oa_version":"Submitted Version","intvolume":" 17","title":"Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions","status":"public","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","_id":"1142"},{"type":"journal_article","publist_id":"6208","issue":"5","abstract":[{"lang":"eng","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."}],"_id":"1150","year":"2016","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publisher":"Cell Press","intvolume":" 38","department":[{"_id":"MiSi"}],"status":"public","title":"A Radical Break Restraining Neutrophil Migration","publication_status":"published","author":[{"first_name":"Jörg","last_name":"Renkawitz","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2856-3369","full_name":"Renkawitz, Jörg"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","first_name":"Michael K","last_name":"Sixt","full_name":"Sixt, Michael K"}],"volume":38,"oa_version":"None","date_updated":"2021-01-12T06:48:39Z","date_created":"2018-12-11T11:50:25Z","scopus_import":1,"day":"12","month":"09","citation":{"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","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.","ista":"Renkawitz J, Sixt MK. 2016. A Radical Break Restraining Neutrophil Migration. Developmental Cell. 38(5), 448–450.","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","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.","short":"J. Renkawitz, M.K. Sixt, Developmental Cell 38 (2016) 448–450.","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."},"publication":"Developmental Cell","page":"448 - 450","quality_controlled":"1","doi":"10.1016/j.devcel.2016.08.017","date_published":"2016-09-12T00:00:00Z","language":[{"iso":"eng"}]},{"_id":"1154","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","intvolume":" 6","ddc":["579"],"status":"public","title":"A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients","pubrep_id":"744","file":[{"file_name":"IST-2017-744-v1+1_srep36440.pdf","access_level":"open_access","creator":"system","content_type":"application/pdf","file_size":2353456,"file_id":"4756","relation":"main_file","date_updated":"2018-12-12T10:09:32Z","date_created":"2018-12-12T10:09:32Z"}],"oa_version":"Published Version","type":"journal_article","abstract":[{"lang":"eng","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"}],"citation":{"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).","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.","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.","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","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","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."},"publication":"Scientific Reports","date_published":"2016-11-07T00:00:00Z","scopus_import":1,"has_accepted_license":"1","day":"07","year":"2016","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","department":[{"_id":"MiSi"},{"_id":"NanoFab"},{"_id":"Bio"},{"_id":"ToBo"}],"publisher":"Nature Publishing Group","publication_status":"published","author":[{"full_name":"Schwarz, Jan","first_name":"Jan","last_name":"Schwarz","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87"},{"id":"3FD04378-F248-11E8-B48F-1D18A9856A87","last_name":"Bierbaum","first_name":"Veronika","full_name":"Bierbaum, Veronika"},{"id":"4515C308-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5145-4609","first_name":"Jack","last_name":"Merrin","full_name":"Merrin, Jack"},{"full_name":"Frank, Tino","first_name":"Tino","last_name":"Frank"},{"id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9843-3522","first_name":"Robert","last_name":"Hauschild","full_name":"Hauschild, Robert"},{"full_name":"Bollenbach, Mark Tobias","last_name":"Bollenbach","first_name":"Mark Tobias","orcid":"0000-0003-4398-476X","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Savaş","last_name":"Tay","full_name":"Tay, Savaş"},{"full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","first_name":"Michael K","last_name":"Sixt"},{"orcid":"0000-0001-8599-1226","id":"3C23B994-F248-11E8-B48F-1D18A9856A87","last_name":"Mehling","first_name":"Matthias","full_name":"Mehling, Matthias"}],"volume":6,"date_updated":"2021-01-12T06:48:41Z","date_created":"2018-12-11T11:50:27Z","article_number":"36440","publist_id":"6204","ec_funded":1,"file_date_updated":"2018-12-12T10:09:32Z","oa":1,"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"project":[{"grant_number":"281556","_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)"},{"_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","grant_number":"Y 564-B12","call_identifier":"FWF","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)"}],"quality_controlled":"1","doi":"10.1038/srep36440","language":[{"iso":"eng"}],"month":"11"},{"type":"journal_article","publist_id":"6149","issue":"6","abstract":[{"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.","lang":"eng"}],"intvolume":" 167","publisher":"Cell Press","department":[{"_id":"MiSi"}],"status":"public","title":"Formin’ a nuclear protection","publication_status":"published","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","_id":"1201","year":"2016","oa_version":"None","volume":167,"date_created":"2018-12-11T11:50:41Z","date_updated":"2021-01-12T06:49:03Z","author":[{"full_name":"Renkawitz, Jörg","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2856-3369","first_name":"Jörg","last_name":"Renkawitz"},{"full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"}],"scopus_import":1,"day":"01","month":"12","page":"1448 - 1449","quality_controlled":"1","citation":{"ista":"Renkawitz J, Sixt MK. 2016. Formin’ a nuclear protection. Cell. 167(6), 1448–1449.","apa":"Renkawitz, J., & Sixt, M. K. (2016). Formin’ a nuclear protection. Cell. Cell Press. https://doi.org/10.1016/j.cell.2016.11.024","ieee":"J. Renkawitz and M. K. Sixt, “Formin’ a nuclear protection,” Cell, vol. 167, no. 6. Cell Press, pp. 1448–1449, 2016.","ama":"Renkawitz J, Sixt MK. Formin’ a nuclear protection. Cell. 2016;167(6):1448-1449. doi:10.1016/j.cell.2016.11.024","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.","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.","short":"J. Renkawitz, M.K. Sixt, Cell 167 (2016) 1448–1449."},"publication":"Cell","language":[{"iso":"eng"}],"doi":"10.1016/j.cell.2016.11.024","date_published":"2016-12-01T00:00:00Z"},{"date_created":"2018-12-11T11:50:46Z","date_updated":"2021-01-12T06:49:09Z","volume":94,"oa_version":"None","author":[{"full_name":"Sreeramkumar, Vinatha","last_name":"Sreeramkumar","first_name":"Vinatha"},{"full_name":"Hons, Miroslav","last_name":"Hons","first_name":"Miroslav","orcid":"0000-0002-6625-3348","id":"4167FE56-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Punzón, Carmen","last_name":"Punzón","first_name":"Carmen"},{"full_name":"Stein, Jens","first_name":"Jens","last_name":"Stein"},{"full_name":"Sancho, David","first_name":"David","last_name":"Sancho"},{"last_name":"Fresno Forcelledo","first_name":"Manuel","full_name":"Fresno Forcelledo, Manuel"},{"full_name":"Cuesta, Natalia","last_name":"Cuesta","first_name":"Natalia"}],"publication_status":"published","status":"public","title":"Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors","intvolume":" 94","department":[{"_id":"MiSi"}],"publisher":"Nature Publishing Group","_id":"1217","year":"2016","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","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.","abstract":[{"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.","lang":"eng"}],"issue":"1","publist_id":"6116","type":"journal_article","language":[{"iso":"eng"}],"date_published":"2016-01-01T00:00:00Z","doi":"10.1038/icb.2015.62","quality_controlled":"1","page":"39 - 51","publication":"Immunology and Cell Biology","citation":{"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.","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","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.","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","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.","short":"V. Sreeramkumar, M. Hons, C. Punzón, J. Stein, D. Sancho, M. Fresno Forcelledo, N. Cuesta, Immunology and Cell Biology 94 (2016) 39–51.","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."},"day":"01","month":"01","scopus_import":1},{"abstract":[{"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.","lang":"eng"}],"ec_funded":1,"publist_id":"6031","type":"journal_article","author":[{"last_name":"Paluch","first_name":"Ewa","full_name":"Paluch, Ewa"},{"last_name":"Aspalter","first_name":"Irene","full_name":"Aspalter, Irene"},{"full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"date_created":"2018-12-11T11:51:08Z","date_updated":"2021-01-12T06:49:37Z","volume":32,"oa_version":"None","year":"2016","_id":"1285","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.).","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","title":"Focal adhesion-independent cell migration","status":"public","publication_status":"published","intvolume":" 32","department":[{"_id":"MiSi"}],"publisher":"Annual Reviews","month":"10","day":"06","scopus_import":1,"doi":"10.1146/annurev-cellbio-111315-125341","date_published":"2016-10-06T00:00:00Z","language":[{"iso":"eng"}],"publication":"Annual Review of Cell and Developmental Biology","citation":{"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.","short":"E. Paluch, I. Aspalter, M.K. Sixt, Annual Review of Cell and Developmental Biology 32 (2016) 469–490.","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","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.","ista":"Paluch E, Aspalter I, Sixt MK. 2016. Focal adhesion-independent cell migration. Annual Review of Cell and Developmental Biology. 32, 469–490.","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"},"quality_controlled":"1","project":[{"grant_number":"281556","_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)"},{"call_identifier":"FWF","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425"}],"page":"469 - 490"},{"file_date_updated":"2020-07-14T12:44:58Z","publist_id":"5697","author":[{"first_name":"Erica","last_name":"Russo","full_name":"Russo, Erica"},{"full_name":"Teijeira, Alvaro","first_name":"Alvaro","last_name":"Teijeira"},{"full_name":"Vaahtomeri, Kari","last_name":"Vaahtomeri","first_name":"Kari","orcid":"0000-0001-7829-3518","id":"368EE576-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Ann","last_name":"Willrodt","full_name":"Willrodt, Ann"},{"first_name":"Joël","last_name":"Bloch","full_name":"Bloch, Joël"},{"last_name":"Nitschké","first_name":"Maximilian","full_name":"Nitschké, Maximilian"},{"first_name":"Laura","last_name":"Santambrogio","full_name":"Santambrogio, Laura"},{"full_name":"Kerjaschki, Dontscho","first_name":"Dontscho","last_name":"Kerjaschki"},{"first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"},{"last_name":"Halin","first_name":"Cornelia","full_name":"Halin, Cornelia"}],"date_updated":"2021-01-12T06:51:07Z","date_created":"2018-12-11T11:52:19Z","volume":14,"year":"2016","publication_status":"published","publisher":"Cell Press","department":[{"_id":"MiSi"}],"month":"02","doi":"10.1016/j.celrep.2016.01.048","language":[{"iso":"eng"}],"tmp":{"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","short":"CC BY-NC-ND (4.0)","image":"/images/cc_by_nc_nd.png"},"oa":1,"quality_controlled":"1","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."}],"issue":"7","type":"journal_article","pubrep_id":"515","oa_version":"Published Version","file":[{"content_type":"application/pdf","file_size":5489897,"creator":"system","file_name":"IST-2016-515-v1+1_1-s2.0-S2211124716300262-main.pdf","access_level":"open_access","date_updated":"2020-07-14T12:44:58Z","date_created":"2018-12-12T10:12:30Z","checksum":"c98c1151d5f1e5ce1643a83d8d7f3c29","relation":"main_file","file_id":"4948"}],"_id":"1490","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","status":"public","ddc":["570"],"title":"Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels","intvolume":" 14","day":"23","has_accepted_license":"1","scopus_import":1,"date_published":"2016-02-23T00:00:00Z","publication":"Cell Reports","citation":{"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.","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.","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.","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","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.","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."},"page":"1723 - 1734"},{"ec_funded":1,"publist_id":"5570","volume":351,"date_updated":"2021-01-12T06:51:52Z","date_created":"2018-12-11T11:52:57Z","author":[{"full_name":"Kiermaier, Eva","first_name":"Eva","last_name":"Kiermaier","id":"3EB04B78-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6165-5738"},{"last_name":"Moussion","first_name":"Christine","id":"3356F664-F248-11E8-B48F-1D18A9856A87","full_name":"Moussion, Christine"},{"full_name":"Veldkamp, Christopher","last_name":"Veldkamp","first_name":"Christopher"},{"first_name":"Rita","last_name":"Gerardy Schahn","full_name":"Gerardy Schahn, Rita"},{"full_name":"De Vries, Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid","last_name":"De Vries"},{"full_name":"Williams, Larry","last_name":"Williams","first_name":"Larry"},{"last_name":"Chaffee","first_name":"Gary","full_name":"Chaffee, Gary"},{"full_name":"Phillips, Andrew","last_name":"Phillips","first_name":"Andrew"},{"full_name":"Freiberger, Friedrich","first_name":"Friedrich","last_name":"Freiberger"},{"last_name":"Imre","first_name":"Richard","full_name":"Imre, Richard"},{"last_name":"Taleski","first_name":"Deni","full_name":"Taleski, Deni"},{"last_name":"Payne","first_name":"Richard","full_name":"Payne, Richard"},{"full_name":"Braun, Asolina","last_name":"Braun","first_name":"Asolina"},{"first_name":"Reinhold","last_name":"Förster","full_name":"Förster, Reinhold"},{"full_name":"Mechtler, Karl","last_name":"Mechtler","first_name":"Karl"},{"first_name":"Martina","last_name":"Mühlenhoff","full_name":"Mühlenhoff, Martina"},{"full_name":"Volkman, Brian","last_name":"Volkman","first_name":"Brian"},{"full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","first_name":"Michael K"}],"department":[{"_id":"MiSi"}],"publisher":"American Association for the Advancement of Science","publication_status":"published","pmid":1,"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. ","year":"2016","month":"01","language":[{"iso":"eng"}],"acknowledged_ssus":[{"_id":"SSU"}],"doi":"10.1126/science.aad0512","project":[{"grant_number":"281556","_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)"},{"name":"Stromal Cell-immune Cell Interactions in Health and Disease","call_identifier":"FP7","_id":"25A76F58-B435-11E9-9278-68D0E5697425","grant_number":"289720"},{"_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","grant_number":"Y 564-B12","call_identifier":"FWF","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)"}],"quality_controlled":"1","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5583642/","open_access":"1"}],"oa":1,"external_id":{"pmid":["26657283"]},"issue":"6269","abstract":[{"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","lang":"eng"}],"type":"journal_article","oa_version":"Submitted Version","intvolume":" 351","title":"Polysialylation controls dendritic cell trafficking by regulating chemokine recognition","status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"1599","article_processing_charge":"No","day":"08","scopus_import":1,"date_published":"2016-01-08T00:00:00Z","page":"186 - 190","article_type":"original","citation":{"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","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","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.","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.","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.","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."},"publication":"Science"},{"day":"01","article_processing_charge":"No","scopus_import":1,"date_published":"2016-01-01T00:00:00Z","article_type":"original","page":"567 - 581","publication":"Methods in Enzymology","citation":{"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.","short":"J. Schwarz, M.K. Sixt, Methods in Enzymology 570 (2016) 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.","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","ista":"Schwarz J, Sixt MK. 2016. Quantitative analysis of dendritic cell haptotaxis. Methods in Enzymology. 570, 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","ieee":"J. Schwarz and M. K. Sixt, “Quantitative analysis of dendritic cell haptotaxis,” Methods in Enzymology, vol. 570. Elsevier, pp. 567–581, 2016."},"abstract":[{"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.","lang":"eng"}],"type":"journal_article","oa_version":"None","title":"Quantitative analysis of dendritic cell haptotaxis","status":"public","intvolume":" 570","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"1597","month":"01","acknowledged_ssus":[{"_id":"Bio"}],"language":[{"iso":"eng"}],"doi":"10.1016/bs.mie.2015.11.004","quality_controlled":"1","project":[{"call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556","_id":"25A603A2-B435-11E9-9278-68D0E5697425"},{"call_identifier":"FWF","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425"}],"external_id":{"pmid":["26921962"]},"ec_funded":1,"publist_id":"5573","date_created":"2018-12-11T11:52:56Z","date_updated":"2021-01-12T06:51:51Z","volume":570,"author":[{"first_name":"Jan","last_name":"Schwarz","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","full_name":"Schwarz, Jan"},{"first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"}],"publication_status":"published","department":[{"_id":"MiSi"}],"publisher":"Elsevier","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.","year":"2016","pmid":1},{"type":"dissertation","alternative_title":["ISTA Thesis"],"abstract":[{"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.","lang":"eng"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","_id":"1129","ddc":["570"],"title":"Quantitative analysis of haptotactic cell migration","status":"public","file":[{"relation":"main_file","file_id":"6813","checksum":"e3cd6b28f9c5cccb8891855565a2dade","date_updated":"2019-08-13T10:55:35Z","date_created":"2019-08-13T10:55:35Z","access_level":"closed","file_name":"Thesis_JSchwarz_final.pdf","file_size":32044069,"content_type":"application/pdf","creator":"dernst"},{"relation":"main_file","file_id":"9181","date_created":"2021-02-22T11:43:14Z","date_updated":"2021-02-22T11:43:14Z","checksum":"c3dbe219acf87eed2f46d21d5cca00de","success":1,"file_name":"2016_Thesis_JSchwarz.pdf","access_level":"open_access","content_type":"application/pdf","file_size":8396717,"creator":"dernst"}],"oa_version":"Published Version","has_accepted_license":"1","article_processing_charge":"No","day":"01","citation":{"chicago":"Schwarz, Jan. “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.","short":"J. Schwarz, Quantitative Analysis of Haptotactic Cell Migration, Institute of Science and Technology Austria, 2016.","ista":"Schwarz J. 2016. Quantitative analysis of haptotactic cell migration. Institute of Science and Technology Austria.","ieee":"J. Schwarz, “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."},"page":"178","date_published":"2016-07-01T00:00:00Z","publist_id":"6231","file_date_updated":"2021-02-22T11:43:14Z","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","year":"2016","department":[{"_id":"MiSi"}],"publisher":"Institute of Science and Technology Austria","publication_status":"published","author":[{"id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","first_name":"Jan","last_name":"Schwarz","full_name":"Schwarz, Jan"}],"date_updated":"2023-09-07T11:54:33Z","date_created":"2018-12-11T11:50:18Z","publication_identifier":{"issn":["2663-337X"]},"month":"07","oa":1,"language":[{"iso":"eng"}],"acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"},{"_id":"LifeSc"}],"degree_awarded":"PhD","supervisor":[{"last_name":"Sixt","first_name":"Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K"}]},{"department":[{"_id":"MiSi"},{"_id":"NanoFab"},{"_id":"Bio"}],"publisher":"Nature Publishing Group","publication_status":"published","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.","year":"2016","volume":18,"date_created":"2018-12-11T11:51:21Z","date_updated":"2024-03-28T23:30:16Z","related_material":{"record":[{"id":"323","relation":"dissertation_contains","status":"public"}]},"author":[{"full_name":"Leithner, Alexander F","first_name":"Alexander F","last_name":"Leithner","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-1073-744X"},{"full_name":"Eichner, Alexander","first_name":"Alexander","last_name":"Eichner","id":"4DFA52AE-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Jan","last_name":"Müller","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D","full_name":"Müller, Jan"},{"last_name":"Reversat","first_name":"Anne","orcid":"0000-0003-0666-8928","id":"35B76592-F248-11E8-B48F-1D18A9856A87","full_name":"Reversat, Anne"},{"full_name":"Brown, Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","first_name":"Markus","last_name":"Brown"},{"id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","last_name":"Schwarz","first_name":"Jan","full_name":"Schwarz, Jan"},{"full_name":"Merrin, Jack","id":"4515C308-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5145-4609","first_name":"Jack","last_name":"Merrin"},{"full_name":"De Gorter, David","last_name":"De Gorter","first_name":"David"},{"full_name":"Schur, Florian","id":"48AD8942-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4790-8078","first_name":"Florian","last_name":"Schur"},{"last_name":"Bayerl","first_name":"Jonathan","full_name":"Bayerl, Jonathan"},{"full_name":"De Vries, Ingrid","first_name":"Ingrid","last_name":"De Vries","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Stefan","last_name":"Wieser","id":"355AA5A0-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-2670-2217","full_name":"Wieser, Stefan"},{"full_name":"Hauschild, Robert","last_name":"Hauschild","first_name":"Robert","orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Frank","last_name":"Lai","full_name":"Lai, Frank"},{"full_name":"Moser, Markus","last_name":"Moser","first_name":"Markus"},{"full_name":"Kerjaschki, Dontscho","last_name":"Kerjaschki","first_name":"Dontscho"},{"full_name":"Rottner, Klemens","first_name":"Klemens","last_name":"Rottner"},{"full_name":"Small, Victor","first_name":"Victor","last_name":"Small"},{"first_name":"Theresia","last_name":"Stradal","full_name":"Stradal, Theresia"},{"first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"}],"license":"https://creativecommons.org/licenses/by-nc-sa/4.0/","ec_funded":1,"publist_id":"5949","file_date_updated":"2020-07-14T12:44:43Z","project":[{"grant_number":"281556","_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)"}],"quality_controlled":"1","oa":1,"tmp":{"name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","image":"/images/cc_by_nc_sa.png","short":"CC BY-NC-SA (4.0)"},"language":[{"iso":"eng"}],"acknowledged_ssus":[{"_id":"SSU"}],"doi":"10.1038/ncb3426","month":"10","intvolume":" 18","ddc":["570"],"status":"public","title":"Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes","_id":"1321","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","oa_version":"Submitted Version","file":[{"file_size":4433280,"content_type":"application/pdf","creator":"dernst","file_name":"2018_NatureCell_Leithner.pdf","access_level":"open_access","date_created":"2020-05-14T16:33:46Z","date_updated":"2020-07-14T12:44:43Z","checksum":"e1411cb7c99a2d9089c178a6abef25e7","relation":"main_file","file_id":"7844"}],"type":"journal_article","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."}],"page":"1253 - 1259","article_type":"original","citation":{"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","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.","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.","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","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.","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.","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."},"publication":"Nature Cell Biology","date_published":"2016-10-24T00:00:00Z","scopus_import":1,"article_processing_charge":"No","has_accepted_license":"1","day":"24"},{"publisher":"IOP Publishing Ltd.","intvolume":" 12","department":[{"_id":"MiSi"}],"status":"public","title":"Impact of the cell division cycle on gene circuits","publication_status":"published","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"1530","year":"2015","oa_version":"None","volume":12,"date_created":"2018-12-11T11:52:33Z","date_updated":"2021-01-12T06:51:25Z","author":[{"full_name":"Bierbaum, Veronika","id":"3FD04378-F248-11E8-B48F-1D18A9856A87","first_name":"Veronika","last_name":"Bierbaum"},{"last_name":"Klumpp","first_name":"Stefan","full_name":"Klumpp, Stefan"}],"type":"journal_article","article_number":"066003","publist_id":"5641","issue":"6","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."}],"quality_controlled":"1","citation":{"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","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.","ista":"Bierbaum V, Klumpp S. 2015. Impact of the cell division cycle on gene circuits. Physical Biology. 12(6), 066003.","short":"V. Bierbaum, S. Klumpp, Physical Biology 12 (2015).","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.","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."},"publication":"Physical Biology","language":[{"iso":"eng"}],"doi":"10.1088/1478-3975/12/6/066003","date_published":"2015-09-25T00:00:00Z","scopus_import":1,"day":"25","month":"09"},{"publication":"Cell","citation":{"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.","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.","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.","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","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.","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","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."},"quality_controlled":"1","project":[{"call_identifier":"FWF","name":"Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation","_id":"2529486C-B435-11E9-9278-68D0E5697425","grant_number":"T 560-B17"},{"call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","_id":"25A603A2-B435-11E9-9278-68D0E5697425","grant_number":"281556"},{"_id":"25ABD200-B435-11E9-9278-68D0E5697425","grant_number":"RGP0058/2011","name":"Cell migration in complex environments: from in vivo experiments to theoretical models"}],"page":"374 - 386","doi":"10.1016/j.cell.2015.01.056","date_published":"2015-04-09T00:00:00Z","language":[{"iso":"eng"}],"scopus_import":1,"month":"04","day":"09","_id":"1553","year":"2015","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_status":"published","status":"public","title":"Actin flows mediate a universal coupling between cell speed and cell persistence","publisher":"Cell Press","intvolume":" 161","department":[{"_id":"MiSi"},{"_id":"CaHe"}],"author":[{"first_name":"Paolo","last_name":"Maiuri","full_name":"Maiuri, Paolo"},{"first_name":"Jean","last_name":"Rupprecht","full_name":"Rupprecht, Jean"},{"full_name":"Wieser, Stefan","orcid":"0000-0002-2670-2217","id":"355AA5A0-F248-11E8-B48F-1D18A9856A87","last_name":"Wieser","first_name":"Stefan"},{"full_name":"Ruprecht, Verena","last_name":"Ruprecht","first_name":"Verena","orcid":"0000-0003-4088-8633","id":"4D71A03A-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Bénichou","first_name":"Olivier","full_name":"Bénichou, Olivier"},{"last_name":"Carpi","first_name":"Nicolas","full_name":"Carpi, Nicolas"},{"full_name":"Coppey, Mathieu","last_name":"Coppey","first_name":"Mathieu"},{"full_name":"De Beco, Simon","last_name":"De Beco","first_name":"Simon"},{"full_name":"Gov, Nir","first_name":"Nir","last_name":"Gov"},{"full_name":"Heisenberg, Carl-Philipp J","last_name":"Heisenberg","first_name":"Carl-Philipp J","orcid":"0000-0002-0912-4566","id":"39427864-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Lage Crespo, Carolina","first_name":"Carolina","last_name":"Lage Crespo"},{"full_name":"Lautenschlaeger, Franziska","last_name":"Lautenschlaeger","first_name":"Franziska"},{"full_name":"Le Berre, Maël","last_name":"Le Berre","first_name":"Maël"},{"first_name":"Ana","last_name":"Lennon Duménil","full_name":"Lennon Duménil, Ana"},{"last_name":"Raab","first_name":"Matthew","full_name":"Raab, Matthew"},{"full_name":"Thiam, Hawa","first_name":"Hawa","last_name":"Thiam"},{"last_name":"Piel","first_name":"Matthieu","full_name":"Piel, Matthieu"},{"last_name":"Sixt","first_name":"Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K"},{"first_name":"Raphaël","last_name":"Voituriez","full_name":"Voituriez, Raphaël"}],"date_created":"2018-12-11T11:52:41Z","date_updated":"2021-01-12T06:51:33Z","volume":161,"oa_version":"None","type":"journal_article","abstract":[{"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.","lang":"eng"}],"ec_funded":1,"publist_id":"5618","issue":"2"},{"publication_status":"published","title":"A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors","status":"public","intvolume":" 45","publisher":"Wiley","department":[{"_id":"MiSi"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"1561","year":"2015","date_updated":"2021-01-12T06:51:36Z","date_created":"2018-12-11T11:52:44Z","volume":45,"oa_version":"None","author":[{"last_name":"Heger","first_name":"Klaus","full_name":"Heger, Klaus"},{"last_name":"Kober","first_name":"Maike","full_name":"Kober, Maike"},{"last_name":"Rieß","first_name":"David","full_name":"Rieß, David"},{"last_name":"Drees","first_name":"Christoph","full_name":"Drees, Christoph"},{"full_name":"De Vries, Ingrid","last_name":"De Vries","first_name":"Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Bertossi, Arianna","last_name":"Bertossi","first_name":"Arianna"},{"full_name":"Roers, Axel","last_name":"Roers","first_name":"Axel"},{"full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","first_name":"Michael K"},{"full_name":"Schmidt Supprian, Marc","last_name":"Schmidt Supprian","first_name":"Marc"}],"type":"journal_article","abstract":[{"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.","lang":"eng"}],"issue":"6","publist_id":"5610","quality_controlled":"1","page":"1614 - 1620","publication":"European Journal of Immunology","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.","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.","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.","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","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.","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.","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"},"language":[{"iso":"eng"}],"doi":"10.1002/eji.201545457","date_published":"2015-06-01T00:00:00Z","scopus_import":1,"month":"06","day":"01"},{"date_updated":"2021-01-12T06:51:36Z","date_created":"2018-12-11T11:52:43Z","volume":16,"oa_version":"None","author":[{"orcid":"0000-0002-6625-3348","id":"4167FE56-F248-11E8-B48F-1D18A9856A87","last_name":"Hons","first_name":"Miroslav","full_name":"Hons, Miroslav"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","first_name":"Michael K","last_name":"Sixt","full_name":"Sixt, Michael K"}],"title":"The lymph node filter revealed","status":"public","publication_status":"published","publisher":"Nature Publishing Group","department":[{"_id":"MiSi"}],"intvolume":" 16","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"1560","year":"2015","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."}],"issue":"4","publist_id":"5611","type":"journal_article","language":[{"iso":"eng"}],"date_published":"2015-03-19T00:00:00Z","doi":"10.1038/ni.3126","quality_controlled":"1","page":"338 - 340","publication":"Nature Immunology","citation":{"short":"M. Hons, M.K. Sixt, Nature Immunology 16 (2015) 338–340.","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.","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.","ama":"Hons M, Sixt MK. The lymph node filter revealed. Nature Immunology. 2015;16(4):338-340. doi:10.1038/ni.3126","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.","apa":"Hons, M., & Sixt, M. K. (2015). The lymph node filter revealed. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3126","ista":"Hons M, Sixt MK. 2015. The lymph node filter revealed. Nature Immunology. 16(4), 338–340."},"day":"19","month":"03","scopus_import":1}]