--- _id: '1142' 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. 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).' author: - first_name: Rui full_name: Martins, Rui last_name: Martins - first_name: Julia full_name: Maier, Julia last_name: Maier - first_name: Anna full_name: Gorki, Anna last_name: Gorki - first_name: Kilian full_name: Huber, Kilian last_name: Huber - first_name: Omar full_name: Sharif, Omar last_name: Sharif - first_name: Philipp full_name: Starkl, Philipp last_name: Starkl - first_name: Simona full_name: Saluzzo, Simona last_name: Saluzzo - first_name: Federica full_name: Quattrone, Federica last_name: Quattrone - first_name: Riem full_name: Gawish, Riem last_name: Gawish - first_name: Karin full_name: Lakovits, Karin last_name: Lakovits - first_name: Michael full_name: Aichinger, Michael last_name: Aichinger - first_name: Branka full_name: Radic Sarikas, Branka last_name: Radic Sarikas - first_name: Charles full_name: Lardeau, Charles last_name: Lardeau - first_name: Anastasiya full_name: Hladik, Anastasiya last_name: Hladik - first_name: Ana full_name: Korosec, Ana last_name: Korosec - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Michelle full_name: Duggan, Michelle id: 2EDEA62C-F248-11E8-B48F-1D18A9856A87 last_name: Duggan - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki - first_name: Harald full_name: Esterbauer, Harald last_name: Esterbauer - first_name: Jacques full_name: Colinge, Jacques last_name: Colinge - first_name: Stephanie full_name: Eisenbarth, Stephanie last_name: Eisenbarth - first_name: Thomas full_name: Decker, Thomas last_name: Decker - first_name: Keiryn full_name: Bennett, Keiryn last_name: Bennett - first_name: Stefan full_name: Kubicek, Stefan last_name: Kubicek - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Giulio full_name: Superti Furga, Giulio last_name: Superti Furga - first_name: Sylvia full_name: Knapp, Sylvia last_name: Knapp citation: 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 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 chicago: Martins, Rui, Julia Maier, Anna Gorki, Kilian Huber, Omar Sharif, Philipp Starkl, Simona Saluzzo, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection via Disruption of Phagocyte Functions.” Nature Immunology. Nature Publishing Group, 2016. https://doi.org/10.1038/ni.3590. ieee: R. Martins et al., “Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions,” Nature Immunology, vol. 17, no. 12. Nature Publishing Group, pp. 1361–1372, 2016. 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. 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. date_created: 2018-12-11T11:50:22Z date_published: 2016-12-01T00:00:00Z date_updated: 2021-01-12T06:48:36Z day: '01' department: - _id: MiSi - _id: PeJo doi: 10.1038/ni.3590 intvolume: ' 17' issue: '12' language: - iso: eng main_file_link: - open_access: '1' url: https://ora.ox.ac.uk/objects/uuid:f53a464e-1e5b-4f08-a7d8-b6749b852b9d month: '12' oa: 1 oa_version: Submitted Version page: 1361 - 1372 publication: Nature Immunology publication_status: published publisher: Nature Publishing Group publist_id: '6216' quality_controlled: '1' scopus_import: 1 status: public title: Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 17 year: '2016' ... --- _id: '1150' 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. author: - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: 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 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 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. 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. 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. short: J. Renkawitz, M.K. Sixt, Developmental Cell 38 (2016) 448–450. date_created: 2018-12-11T11:50:25Z date_published: 2016-09-12T00:00:00Z date_updated: 2021-01-12T06:48:39Z day: '12' department: - _id: MiSi doi: 10.1016/j.devcel.2016.08.017 intvolume: ' 38' issue: '5' language: - iso: eng month: '09' oa_version: None page: 448 - 450 publication: Developmental Cell publication_status: published publisher: Cell Press publist_id: '6208' quality_controlled: '1' scopus_import: 1 status: public title: A Radical Break Restraining Neutrophil Migration type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 38 year: '2016' ... --- _id: '1154' 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" 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' article_number: '36440' author: - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Veronika full_name: Bierbaum, Veronika id: 3FD04378-F248-11E8-B48F-1D18A9856A87 last_name: Bierbaum - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Tino full_name: Frank, Tino last_name: Frank - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Mark Tobias full_name: Bollenbach, Mark Tobias id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87 last_name: Bollenbach orcid: 0000-0003-4398-476X - first_name: Savaş full_name: Tay, Savaş last_name: Tay - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Matthias full_name: Mehling, Matthias id: 3C23B994-F248-11E8-B48F-1D18A9856A87 last_name: Mehling orcid: 0000-0001-8599-1226 citation: 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 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 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. 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. ista: Schwarz J, Bierbaum V, Merrin J, Frank T, Hauschild R, Bollenbach MT, Tay S, Sixt MK, Mehling M. 2016. A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients. Scientific Reports. 6, 36440. mla: Schwarz, Jan, et al. “A Microfluidic Device for Measuring Cell Migration towards Substrate Bound and Soluble Chemokine Gradients.” Scientific Reports, vol. 6, 36440, Nature Publishing Group, 2016, doi:10.1038/srep36440. short: J. Schwarz, V. Bierbaum, J. Merrin, T. Frank, R. Hauschild, M.T. Bollenbach, S. Tay, M.K. Sixt, M. Mehling, Scientific Reports 6 (2016). date_created: 2018-12-11T11:50:27Z date_published: 2016-11-07T00:00:00Z date_updated: 2021-01-12T06:48:41Z day: '07' ddc: - '579' department: - _id: MiSi - _id: NanoFab - _id: Bio - _id: ToBo doi: 10.1038/srep36440 ec_funded: 1 file: - access_level: open_access content_type: application/pdf creator: system date_created: 2018-12-12T10:09:32Z date_updated: 2018-12-12T10:09:32Z file_id: '4756' file_name: IST-2017-744-v1+1_srep36440.pdf file_size: 2353456 relation: main_file file_date_updated: 2018-12-12T10:09:32Z has_accepted_license: '1' intvolume: ' 6' language: - iso: eng month: '11' oa: 1 oa_version: Published Version project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Scientific Reports publication_status: published publisher: Nature Publishing Group publist_id: '6204' pubrep_id: '744' quality_controlled: '1' scopus_import: 1 status: public title: A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 6 year: '2016' ... --- _id: '1201' abstract: - lang: eng text: In this issue of Cell, Skau et al. show that the formin FMN2 organizes a perinuclear actin cytoskeleton that protects the nucleus and its genomic content of migrating cells squeezing through small spaces. author: - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Renkawitz J, Sixt MK. Formin’ a nuclear protection. Cell. 2016;167(6):1448-1449. doi:10.1016/j.cell.2016.11.024 apa: Renkawitz, J., & Sixt, M. K. (2016). Formin’ a nuclear protection. Cell. Cell Press. https://doi.org/10.1016/j.cell.2016.11.024 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. ieee: J. Renkawitz and M. K. Sixt, “Formin’ a nuclear protection,” Cell, vol. 167, no. 6. Cell Press, pp. 1448–1449, 2016. ista: Renkawitz J, Sixt MK. 2016. Formin’ a nuclear protection. Cell. 167(6), 1448–1449. mla: Renkawitz, Jörg, and Michael K. Sixt. “Formin’ a Nuclear Protection.” Cell, vol. 167, no. 6, Cell Press, 2016, pp. 1448–49, doi:10.1016/j.cell.2016.11.024. short: J. Renkawitz, M.K. Sixt, Cell 167 (2016) 1448–1449. date_created: 2018-12-11T11:50:41Z date_published: 2016-12-01T00:00:00Z date_updated: 2021-01-12T06:49:03Z day: '01' department: - _id: MiSi doi: 10.1016/j.cell.2016.11.024 intvolume: ' 167' issue: '6' language: - iso: eng month: '12' oa_version: None page: 1448 - 1449 publication: Cell publication_status: published publisher: Cell Press publist_id: '6149' quality_controlled: '1' scopus_import: 1 status: public title: Formin’ a nuclear protection type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 167 year: '2016' ... --- _id: '1217' abstract: - lang: eng text: Understanding the regulation of T-cell responses during inflammation and auto-immunity is fundamental for designing efficient therapeutic strategies against immune diseases. In this regard, prostaglandin E 2 (PGE 2) is mostly considered a myeloid-derived immunosuppressive molecule. We describe for the first time that T cells secrete PGE 2 during T-cell receptor stimulation. In addition, we show that autocrine PGE 2 signaling through EP receptors is essential for optimal CD4 + T-cell activation in vitro and in vivo, and for T helper 1 (Th1) and regulatory T cell differentiation. PGE 2 was found to provide additive co-stimulatory signaling through AKT activation. Intravital multiphoton microscopy showed that triggering EP receptors in T cells is also essential for the stability of T cell-dendritic cell (DC) interactions and Th-cell accumulation in draining lymph nodes (LNs) during inflammation. We further demonstrated that blocking EP receptors in T cells during the initial phase of collagen-induced arthritis in mice resulted in a reduction of clinical arthritis. This could be attributable to defective T-cell activation, accompanied by a decline in activated and interferon-γ-producing CD4 + Th1 cells in draining LNs. In conclusion, we prove that T lymphocytes secret picomolar concentrations of PGE 2, which in turn provide additive co-stimulatory signaling, enabling T cells to attain a favorable activation threshold. PGE 2 signaling in T cells is also required for maintaining long and stable interactions with DCs within LNs. Blockade of EP receptors in vivo impairs T-cell activation and development of T cell-mediated inflammatory responses. This may have implications in various pathophysiological settings. 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. author: - first_name: Vinatha full_name: Sreeramkumar, Vinatha last_name: Sreeramkumar - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Carmen full_name: Punzón, Carmen last_name: Punzón - first_name: Jens full_name: Stein, Jens last_name: Stein - first_name: David full_name: Sancho, David last_name: Sancho - first_name: Manuel full_name: Fresno Forcelledo, Manuel last_name: Fresno Forcelledo - first_name: Natalia full_name: Cuesta, Natalia last_name: Cuesta citation: ama: Sreeramkumar V, Hons M, Punzón C, et al. Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors. Immunology and Cell Biology. 2016;94(1):39-51. doi:10.1038/icb.2015.62 apa: Sreeramkumar, V., Hons, M., Punzón, C., Stein, J., Sancho, D., Fresno Forcelledo, M., & Cuesta, N. (2016). Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors. Immunology and Cell Biology. Nature Publishing Group. https://doi.org/10.1038/icb.2015.62 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. 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. 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. 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. short: V. Sreeramkumar, M. Hons, C. Punzón, J. Stein, D. Sancho, M. Fresno Forcelledo, N. Cuesta, Immunology and Cell Biology 94 (2016) 39–51. date_created: 2018-12-11T11:50:46Z date_published: 2016-01-01T00:00:00Z date_updated: 2021-01-12T06:49:09Z day: '01' department: - _id: MiSi doi: 10.1038/icb.2015.62 intvolume: ' 94' issue: '1' language: - iso: eng month: '01' oa_version: None page: 39 - 51 publication: Immunology and Cell Biology publication_status: published publisher: Nature Publishing Group publist_id: '6116' quality_controlled: '1' scopus_import: 1 status: public title: Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 94 year: '2016' ... --- _id: '1285' abstract: - lang: eng text: Cell migration is central to a multitude of physiological processes, including embryonic development, immune surveillance, and wound healing, and deregulated migration is key to cancer dissemination. Decades of investigations have uncovered many of the molecular and physical mechanisms underlying cell migration. Together with protrusion extension and cell body retraction, adhesion to the substrate via specific focal adhesion points has long been considered an essential step in cell migration. Although this is true for cells moving on two-dimensional substrates, recent studies have demonstrated that focal adhesions are not required for cells moving in three dimensions, in which confinement is sufficient to maintain a cell in contact with its substrate. Here, we review the investigations that have led to challenging the requirement of specific adhesions for migration, discuss the physical mechanisms proposed for cell body translocation during focal adhesion-independent migration, and highlight the remaining open questions for the future. acknowledgement: We would like to thank Dani Bodor for critical comments on the manuscript and Guillaume Salbreux for discussions. The authors are supported by the United Kingdom's Medical Research Council (MRC) (E.K.P. and I.M.A.; core funding to the MRC Laboratory for Molecular Cell Biology), by the European Research Council [ERC GA 311637 (E.K.P.) and ERC GA 281556 (M.S.)], and by a START award from the Austrian Science Foundation (M.S.). author: - first_name: Ewa full_name: Paluch, Ewa last_name: Paluch - first_name: Irene full_name: Aspalter, Irene last_name: Aspalter - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: 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 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 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. 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. 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. short: E. Paluch, I. Aspalter, M.K. Sixt, Annual Review of Cell and Developmental Biology 32 (2016) 469–490. date_created: 2018-12-11T11:51:08Z date_published: 2016-10-06T00:00:00Z date_updated: 2021-01-12T06:49:37Z day: '06' department: - _id: MiSi doi: 10.1146/annurev-cellbio-111315-125341 ec_funded: 1 intvolume: ' 32' language: - iso: eng month: '10' oa_version: None page: 469 - 490 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Annual Review of Cell and Developmental Biology publication_status: published publisher: Annual Reviews publist_id: '6031' quality_controlled: '1' scopus_import: 1 status: public title: Focal adhesion-independent cell migration type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 32 year: '2016' ... --- _id: '1490' 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. author: - first_name: Erica full_name: Russo, Erica last_name: Russo - first_name: Alvaro full_name: Teijeira, Alvaro last_name: Teijeira - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Ann full_name: Willrodt, Ann last_name: Willrodt - first_name: Joël full_name: Bloch, Joël last_name: Bloch - first_name: Maximilian full_name: Nitschké, Maximilian last_name: Nitschké - first_name: Laura full_name: Santambrogio, Laura last_name: Santambrogio - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Cornelia full_name: Halin, Cornelia last_name: Halin citation: ama: Russo E, Teijeira A, Vaahtomeri K, et al. Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels. Cell Reports. 2016;14(7):1723-1734. doi:10.1016/j.celrep.2016.01.048 apa: Russo, E., Teijeira, A., Vaahtomeri, K., Willrodt, A., Bloch, J., Nitschké, M., … Halin, C. (2016). Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2016.01.048 chicago: Russo, Erica, Alvaro Teijeira, Kari Vaahtomeri, Ann Willrodt, Joël Bloch, Maximilian Nitschké, Laura Santambrogio, Dontscho Kerjaschki, Michael K Sixt, and Cornelia Halin. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic Cells through Afferent Lymphatic Vessels.” Cell Reports. Cell Press, 2016. https://doi.org/10.1016/j.celrep.2016.01.048. 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. mla: Russo, Erica, et al. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic Cells through Afferent Lymphatic Vessels.” Cell Reports, vol. 14, no. 7, Cell Press, 2016, pp. 1723–34, doi:10.1016/j.celrep.2016.01.048. short: E. Russo, A. Teijeira, K. Vaahtomeri, A. Willrodt, J. Bloch, M. Nitschké, L. Santambrogio, D. Kerjaschki, M.K. Sixt, C. Halin, Cell Reports 14 (2016) 1723–1734. date_created: 2018-12-11T11:52:19Z date_published: 2016-02-23T00:00:00Z date_updated: 2021-01-12T06:51:07Z day: '23' ddc: - '570' department: - _id: MiSi doi: 10.1016/j.celrep.2016.01.048 file: - access_level: open_access checksum: c98c1151d5f1e5ce1643a83d8d7f3c29 content_type: application/pdf creator: system date_created: 2018-12-12T10:12:30Z date_updated: 2020-07-14T12:44:58Z file_id: '4948' file_name: IST-2016-515-v1+1_1-s2.0-S2211124716300262-main.pdf file_size: 5489897 relation: main_file file_date_updated: 2020-07-14T12:44:58Z has_accepted_license: '1' intvolume: ' 14' issue: '7' language: - iso: eng month: '02' oa: 1 oa_version: Published Version page: 1723 - 1734 publication: Cell Reports publication_status: published publisher: Cell Press publist_id: '5697' pubrep_id: '515' quality_controlled: '1' scopus_import: 1 status: public title: Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 14 year: '2016' ... --- _id: '1599' abstract: - lang: eng text: "The addition of polysialic acid to N- and/or O-linked glycans, referred to as polysialylation, is a rare posttranslational modification that is mainly known to control the developmental plasticity of the nervous system. Here we show that CCR7, the central chemokine receptor controlling immune cell trafficking to secondary lymphatic organs, carries polysialic acid. This modification is essential for the recognition of the CCR7 ligand CCL21. As a consequence, dendritic cell trafficking is abrogated in polysialyltransferase-deficient mice, manifesting as disturbed lymph node homeostasis and unresponsiveness to inflammatory stimuli. Structure-function analysis of chemokine-receptor interactions reveals that CCL21 adopts an autoinhibited conformation, which is released upon interaction with polysialic acid. Thus, we describe a glycosylation-mediated immune cell trafficking disorder and its mechanistic basis.\r\n" acknowledged_ssus: - _id: SSU 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. ' article_processing_charge: No article_type: original author: - first_name: Eva full_name: Kiermaier, Eva id: 3EB04B78-F248-11E8-B48F-1D18A9856A87 last_name: Kiermaier orcid: 0000-0001-6165-5738 - first_name: Christine full_name: Moussion, Christine id: 3356F664-F248-11E8-B48F-1D18A9856A87 last_name: Moussion - first_name: Christopher full_name: Veldkamp, Christopher last_name: Veldkamp - first_name: Rita full_name: Gerardy Schahn, Rita last_name: Gerardy Schahn - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Larry full_name: Williams, Larry last_name: Williams - first_name: Gary full_name: Chaffee, Gary last_name: Chaffee - first_name: Andrew full_name: Phillips, Andrew last_name: Phillips - first_name: Friedrich full_name: Freiberger, Friedrich last_name: Freiberger - first_name: Richard full_name: Imre, Richard last_name: Imre - first_name: Deni full_name: Taleski, Deni last_name: Taleski - first_name: Richard full_name: Payne, Richard last_name: Payne - first_name: Asolina full_name: Braun, Asolina last_name: Braun - first_name: Reinhold full_name: Förster, Reinhold last_name: Förster - first_name: Karl full_name: Mechtler, Karl last_name: Mechtler - first_name: Martina full_name: Mühlenhoff, Martina last_name: Mühlenhoff - first_name: Brian full_name: Volkman, Brian last_name: Volkman - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 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 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 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. 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. 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. 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. 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. date_created: 2018-12-11T11:52:57Z date_published: 2016-01-08T00:00:00Z date_updated: 2021-01-12T06:51:52Z day: '08' department: - _id: MiSi doi: 10.1126/science.aad0512 ec_funded: 1 external_id: pmid: - '26657283' intvolume: ' 351' issue: '6269' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5583642/ month: '01' oa: 1 oa_version: Submitted Version page: 186 - 190 pmid: 1 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A76F58-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '289720' name: Stromal Cell-immune Cell Interactions in Health and Disease - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Science publication_status: published publisher: American Association for the Advancement of Science publist_id: '5570' quality_controlled: '1' scopus_import: 1 status: public title: Polysialylation controls dendritic cell trafficking by regulating chemokine recognition type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 351 year: '2016' ... --- _id: '1597' abstract: - lang: eng text: Chemokines are the main guidance cues directing leukocyte migration. Opposed to early assumptions, chemokines do not necessarily act as soluble cues but are often immobilized within tissues, e.g., dendritic cell migration toward lymphatic vessels is guided by a haptotactic gradient of the chemokine CCL21. Controlled assay systems to quantitatively study haptotaxis in vitro are still missing. In this chapter, we describe an in vitro haptotaxis assay optimized for the unique properties of dendritic cells. The chemokine CCL21 is immobilized in a bioactive state, using laser-assisted protein adsorption by photobleaching. The cells follow this immobilized CCL21 gradient in a haptotaxis chamber, which provides three dimensionally confined migration conditions. acknowledged_ssus: - _id: Bio 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. article_processing_charge: No article_type: original author: - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: 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 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 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. ieee: J. Schwarz and M. K. Sixt, “Quantitative analysis of dendritic cell haptotaxis,” Methods in Enzymology, vol. 570. Elsevier, pp. 567–581, 2016. ista: Schwarz J, Sixt MK. 2016. Quantitative analysis of dendritic cell haptotaxis. Methods in Enzymology. 570, 567–581. 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. date_created: 2018-12-11T11:52:56Z date_published: 2016-01-01T00:00:00Z date_updated: 2021-01-12T06:51:51Z day: '01' department: - _id: MiSi doi: 10.1016/bs.mie.2015.11.004 ec_funded: 1 external_id: pmid: - '26921962' intvolume: ' 570' language: - iso: eng month: '01' oa_version: None page: 567 - 581 pmid: 1 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Methods in Enzymology publication_status: published publisher: Elsevier publist_id: '5573' quality_controlled: '1' scopus_import: 1 status: public title: Quantitative analysis of dendritic cell haptotaxis type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 570 year: '2016' ... --- _id: '1129' abstract: - lang: eng text: "Directed cell migration is a hallmark feature, present in almost all multi-cellular\r\norganisms. Despite its importance, basic questions regarding force transduction\r\nor directional sensing are still heavily investigated. Directed migration of cells\r\nguided by immobilized guidance cues - haptotaxis - occurs in key-processes,\r\nsuch as embryonic development and immunity (Middleton et al., 1997; Nguyen\r\net al., 2000; Thiery, 1984; Weber et al., 2013). Immobilized guidance cues\r\ncomprise adhesive ligands, such as collagen and fibronectin (Barczyk et al.,\r\n2009), or chemokines - the main guidance cues for migratory leukocytes\r\n(Middleton et al., 1997; Weber et al., 2013). While adhesive ligands serve as\r\nattachment sites guiding cell migration (Carter, 1965), chemokines instruct\r\nhaptotactic migration by inducing adhesion to adhesive ligands and directional\r\nguidance (Rot and Andrian, 2004; Schumann et al., 2010). Quantitative analysis\r\nof the cellular response to immobilized guidance cues requires in vitro assays\r\nthat foster cell migration, offer accurate control of the immobilized cues on a\r\nsubcellular scale and in the ideal case closely reproduce in vivo conditions. The\r\nexploration of haptotactic cell migration through design and employment of such\r\nassays represents the main focus of this work.\r\nDendritic cells (DCs) are leukocytes, which after encountering danger\r\nsignals such as pathogens in peripheral organs instruct naïve T-cells and\r\nconsequently the adaptive immune response in the lymph node (Mellman and\r\nSteinman, 2001). To reach the lymph node from the periphery, DCs follow\r\nhaptotactic gradients of the chemokine CCL21 towards lymphatic vessels\r\n(Weber et al., 2013). Questions about how DCs interpret haptotactic CCL21\r\ngradients have not yet been addressed. The main reason for this is the lack of\r\nan assay that offers diverse haptotactic environments, hence allowing the study\r\nof DC migration as a response to different signals of immobilized guidance cue.\r\nIn this work, we developed an in vitro assay that enables us to\r\nquantitatively assess DC haptotaxis, by combining precisely controllable\r\nchemokine photo-patterning with physically confining migration conditions. With this tool at hand, we studied the influence of CCL21 gradient properties and\r\nconcentration on DC haptotaxis. We found that haptotactic gradient sensing\r\ndepends on the absolute CCL21 concentration in combination with the local\r\nsteepness of the gradient. Our analysis suggests that the directionality of\r\nmigrating DCs is governed by the signal-to-noise ratio of CCL21 binding to its\r\nreceptor CCR7. Moreover, the haptotactic CCL21 gradient formed in vivo\r\nprovides an optimal shape for DCs to recognize haptotactic guidance cue.\r\nBy reconstitution of the CCL21 gradient in vitro we were also able to\r\nstudy the influence of CCR7 signal termination on DC haptotaxis. To this end,\r\nwe used DCs lacking the G-protein coupled receptor kinase GRK6, which is\r\nresponsible for CCL21 induced CCR7 receptor phosphorylation and\r\ndesensitization (Zidar et al., 2009). We found that CCR7 desensitization by\r\nGRK6 is crucial for maintenance of haptotactic CCL21 gradient sensing in vitro\r\nand confirm those observations in vivo.\r\nIn the context of the organism, immobilized haptotactic guidance cues\r\noften coincide and compete with soluble chemotactic guidance cues. During\r\nwound healing, fibroblasts are exposed and influenced by adhesive cues and\r\nsoluble factors at the same time (Wu et al., 2012; Wynn, 2008). Similarly,\r\nmigrating DCs are exposed to both, soluble chemokines (CCL19 and truncated\r\nCCL21) inducing chemotactic behavior as well as the immobilized CCL21. To\r\nquantitatively assess these complex coinciding immobilized and soluble\r\nguidance cues, we implemented our chemokine photo-patterning technique in a\r\nmicrofluidic system allowing for chemotactic gradient generation. To validate\r\nthe assay, we observed DC migration in competing CCL19/CCL21\r\nenvironments.\r\nAdhesiveness guided haptotaxis has been studied intensively over the\r\nlast century. However, quantitative studies leading to conceptual models are\r\nlargely missing, again due to the lack of a precisely controllable in vitro assay. A\r\nrequirement for such an in vitro assay is that it must prevent any uncontrolled\r\ncell adhesion. This can be accomplished by stable passivation of the surface. In\r\naddition, controlled adhesion must be sustainable, quantifiable and dose\r\ndependent in order to create homogenous gradients. Therefore, we developed a novel covalent photo-patterning technique satisfying all these needs. In\r\ncombination with a sustainable poly-vinyl alcohol (PVA) surface coating we\r\nwere able to generate gradients of adhesive cue to direct cell migration. This\r\napproach allowed us to characterize the haptotactic migratory behavior of\r\nzebrafish keratocytes in vitro. Furthermore, defined patterns of adhesive cue\r\nallowed us to control for cell shape and growth on a subcellular scale." acknowledged_ssus: - _id: Bio - _id: PreCl - _id: LifeSc 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" alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz citation: ama: Schwarz J. Quantitative analysis of haptotactic cell migration. 2016. apa: Schwarz, J. (2016). Quantitative analysis of haptotactic cell migration. Institute of Science and Technology Austria. chicago: Schwarz, Jan. “Quantitative Analysis of Haptotactic Cell Migration.” Institute of Science and Technology Austria, 2016. ieee: 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. 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. date_created: 2018-12-11T11:50:18Z date_published: 2016-07-01T00:00:00Z date_updated: 2023-09-07T11:54:33Z day: '01' ddc: - '570' degree_awarded: PhD department: - _id: MiSi file: - access_level: closed checksum: e3cd6b28f9c5cccb8891855565a2dade content_type: application/pdf creator: dernst date_created: 2019-08-13T10:55:35Z date_updated: 2019-08-13T10:55:35Z file_id: '6813' file_name: Thesis_JSchwarz_final.pdf file_size: 32044069 relation: main_file - access_level: open_access checksum: c3dbe219acf87eed2f46d21d5cca00de content_type: application/pdf creator: dernst date_created: 2021-02-22T11:43:14Z date_updated: 2021-02-22T11:43:14Z file_id: '9181' file_name: 2016_Thesis_JSchwarz.pdf file_size: 8396717 relation: main_file success: 1 file_date_updated: 2021-02-22T11:43:14Z has_accepted_license: '1' language: - iso: eng month: '07' oa: 1 oa_version: Published Version page: '178' publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria publist_id: '6231' status: public supervisor: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 title: Quantitative analysis of haptotactic cell migration type: dissertation user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 year: '2016' ... --- _id: '1321' 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. acknowledged_ssus: - _id: SSU 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." article_processing_charge: No article_type: original author: - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Alexander full_name: Eichner, Alexander id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87 last_name: Eichner - first_name: Jan full_name: Müller, Jan id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D last_name: Müller - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: David full_name: De Gorter, David last_name: De Gorter - first_name: Florian full_name: Schur, Florian id: 48AD8942-F248-11E8-B48F-1D18A9856A87 last_name: Schur orcid: 0000-0003-4790-8078 - first_name: Jonathan full_name: Bayerl, Jonathan last_name: Bayerl - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Stefan full_name: Wieser, Stefan id: 355AA5A0-F248-11E8-B48F-1D18A9856A87 last_name: Wieser orcid: 0000-0002-2670-2217 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Frank full_name: Lai, Frank last_name: Lai - first_name: Markus full_name: Moser, Markus last_name: Moser - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner - first_name: Victor full_name: Small, Victor last_name: Small - first_name: Theresia full_name: Stradal, Theresia last_name: Stradal - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Leithner AF, Eichner A, Müller J, et al. Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. 2016;18:1253-1259. doi:10.1038/ncb3426 apa: Leithner, A. F., Eichner, A., Müller, J., Reversat, A., Brown, M., Schwarz, J., … Sixt, M. K. (2016). Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb3426 chicago: Leithner, Alexander F, Alexander Eichner, Jan Müller, Anne Reversat, Markus Brown, Jan Schwarz, Jack Merrin, et al. “Diversified Actin Protrusions Promote Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature Cell Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/ncb3426. ieee: A. F. Leithner et al., “Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes,” Nature Cell Biology, vol. 18. Nature Publishing Group, pp. 1253–1259, 2016. 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. 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. 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. date_created: 2018-12-11T11:51:21Z date_published: 2016-10-24T00:00:00Z date_updated: 2024-03-27T23:30:16Z day: '24' ddc: - '570' department: - _id: MiSi - _id: NanoFab - _id: Bio doi: 10.1038/ncb3426 ec_funded: 1 file: - access_level: open_access checksum: e1411cb7c99a2d9089c178a6abef25e7 content_type: application/pdf creator: dernst date_created: 2020-05-14T16:33:46Z date_updated: 2020-07-14T12:44:43Z file_id: '7844' file_name: 2018_NatureCell_Leithner.pdf file_size: 4433280 relation: main_file file_date_updated: 2020-07-14T12:44:43Z has_accepted_license: '1' intvolume: ' 18' language: - iso: eng license: https://creativecommons.org/licenses/by-nc-sa/4.0/ month: '10' oa: 1 oa_version: Submitted Version page: 1253 - 1259 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Nature Cell Biology publication_status: published publisher: Nature Publishing Group publist_id: '5949' quality_controlled: '1' related_material: record: - id: '323' relation: dissertation_contains status: public scopus_import: 1 status: public title: Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 18 year: '2016' ... --- _id: '1530' 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. article_number: '066003' author: - first_name: Veronika full_name: Bierbaum, Veronika id: 3FD04378-F248-11E8-B48F-1D18A9856A87 last_name: Bierbaum - first_name: Stefan full_name: Klumpp, Stefan last_name: Klumpp 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 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. 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. 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. short: V. Bierbaum, S. Klumpp, Physical Biology 12 (2015). date_created: 2018-12-11T11:52:33Z date_published: 2015-09-25T00:00:00Z date_updated: 2021-01-12T06:51:25Z day: '25' department: - _id: MiSi doi: 10.1088/1478-3975/12/6/066003 intvolume: ' 12' issue: '6' language: - iso: eng month: '09' oa_version: None publication: Physical Biology publication_status: published publisher: IOP Publishing Ltd. publist_id: '5641' quality_controlled: '1' scopus_import: 1 status: public title: Impact of the cell division cycle on gene circuits type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 12 year: '2015' ... --- _id: '1553' abstract: - lang: eng text: Cell movement has essential functions in development, immunity, and cancer. Various cell migration patterns have been reported, but no general rule has emerged so far. Here, we show on the basis of experimental data in vitro and in vivo that cell persistence, which quantifies the straightness of trajectories, is robustly coupled to cell migration speed. We suggest that this universal coupling constitutes a generic law of cell migration, which originates in the advection of polarity cues by an actin cytoskeleton undergoing flows at the cellular scale. Our analysis relies on a theoretical model that we validate by measuring the persistence of cells upon modulation of actin flow speeds and upon optogenetic manipulation of the binding of an actin regulator to actin filaments. Beyond the quantitative prediction of the coupling, the model yields a generic phase diagram of cellular trajectories, which recapitulates the full range of observed migration patterns. author: - first_name: Paolo full_name: Maiuri, Paolo last_name: Maiuri - first_name: Jean full_name: Rupprecht, Jean last_name: Rupprecht - first_name: Stefan full_name: Wieser, Stefan id: 355AA5A0-F248-11E8-B48F-1D18A9856A87 last_name: Wieser orcid: 0000-0002-2670-2217 - first_name: Verena full_name: Ruprecht, Verena id: 4D71A03A-F248-11E8-B48F-1D18A9856A87 last_name: Ruprecht orcid: 0000-0003-4088-8633 - first_name: Olivier full_name: Bénichou, Olivier last_name: Bénichou - first_name: Nicolas full_name: Carpi, Nicolas last_name: Carpi - first_name: Mathieu full_name: Coppey, Mathieu last_name: Coppey - first_name: Simon full_name: De Beco, Simon last_name: De Beco - first_name: Nir full_name: Gov, Nir last_name: Gov - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 - first_name: Carolina full_name: Lage Crespo, Carolina last_name: Lage Crespo - first_name: Franziska full_name: Lautenschlaeger, Franziska last_name: Lautenschlaeger - first_name: Maël full_name: Le Berre, Maël last_name: Le Berre - first_name: Ana full_name: Lennon Duménil, Ana last_name: Lennon Duménil - first_name: Matthew full_name: Raab, Matthew last_name: Raab - first_name: Hawa full_name: Thiam, Hawa last_name: Thiam - first_name: Matthieu full_name: Piel, Matthieu last_name: Piel - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Raphaël full_name: Voituriez, Raphaël last_name: Voituriez citation: 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 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 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. 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. 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. 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. date_created: 2018-12-11T11:52:41Z date_published: 2015-04-09T00:00:00Z date_updated: 2021-01-12T06:51:33Z day: '09' department: - _id: MiSi - _id: CaHe doi: 10.1016/j.cell.2015.01.056 ec_funded: 1 intvolume: ' 161' issue: '2' language: - iso: eng month: '04' oa_version: None page: 374 - 386 project: - _id: 2529486C-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T 560-B17 name: Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25ABD200-B435-11E9-9278-68D0E5697425 grant_number: RGP0058/2011 name: 'Cell migration in complex environments: from in vivo experiments to theoretical models' publication: Cell publication_status: published publisher: Cell Press publist_id: '5618' quality_controlled: '1' scopus_import: 1 status: public title: Actin flows mediate a universal coupling between cell speed and cell persistence type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 161 year: '2015' ... --- _id: '1561' abstract: - lang: eng text: Replication-deficient recombinant adenoviruses are potent vectors for the efficient transient expression of exogenous genes in resting immune cells. However, most leukocytes are refractory to efficient adenoviral transduction as they lack expression of the coxsackie/adenovirus receptor (CAR). To circumvent this obstacle, we generated the R26/CAG-CARΔ1StopF (where R26 is ROSA26 and CAG is CMV early enhancer/chicken β actin promoter) knock-in mouse line. This strain allows monitoring of in situ Cre recombinase activity through expression of CARΔ1. Simultaneously, CARΔ1 expression permits selective and highly efficient adenoviral transduction of immune cell populations, such as mast cells or T cells, directly ex vivo in bulk cultures without prior cell purification or activation. Furthermore, we show that CARΔ1 expression dramatically improves adenoviral infection of in vitro differentiated conventional and plasmacytoid dendritic cells (DCs), basophils, mast cells, as well as Hoxb8-immortalized hematopoietic progenitor cells. This novel dual function mouse strain will hence be a valuable tool to rapidly dissect the function of specific genes in leukocyte physiology. author: - first_name: Klaus full_name: Heger, Klaus last_name: Heger - first_name: Maike full_name: Kober, Maike last_name: Kober - first_name: David full_name: Rieß, David last_name: Rieß - first_name: Christoph full_name: Drees, Christoph last_name: Drees - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Arianna full_name: Bertossi, Arianna last_name: Bertossi - first_name: Axel full_name: Roers, Axel last_name: Roers - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Marc full_name: Schmidt Supprian, Marc last_name: Schmidt Supprian citation: 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 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 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. 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. 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. 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. date_created: 2018-12-11T11:52:44Z date_published: 2015-06-01T00:00:00Z date_updated: 2021-01-12T06:51:36Z day: '01' department: - _id: MiSi doi: 10.1002/eji.201545457 intvolume: ' 45' issue: '6' language: - iso: eng month: '06' oa_version: None page: 1614 - 1620 publication: European Journal of Immunology publication_status: published publisher: Wiley publist_id: '5610' quality_controlled: '1' scopus_import: 1 status: public title: A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 45 year: '2015' ... --- _id: '1560' 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. author: - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Hons M, Sixt MK. The lymph node filter revealed. Nature Immunology. 2015;16(4):338-340. doi:10.1038/ni.3126 apa: Hons, M., & Sixt, M. K. (2015). The lymph node filter revealed. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3126 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. 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. ista: Hons M, Sixt MK. 2015. The lymph node filter revealed. Nature Immunology. 16(4), 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. short: M. Hons, M.K. Sixt, Nature Immunology 16 (2015) 338–340. date_created: 2018-12-11T11:52:43Z date_published: 2015-03-19T00:00:00Z date_updated: 2021-01-12T06:51:36Z day: '19' department: - _id: MiSi doi: 10.1038/ni.3126 intvolume: ' 16' issue: '4' language: - iso: eng month: '03' oa_version: None page: 338 - 340 publication: Nature Immunology publication_status: published publisher: Nature Publishing Group publist_id: '5611' quality_controlled: '1' scopus_import: 1 status: public title: The lymph node filter revealed type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 16 year: '2015' ... --- _id: '1575' abstract: - lang: eng text: The immune response relies on the migration of leukocytes and on their ability to stop in precise anatomical locations to fulfil their task. How leukocyte migration and function are coordinated is unknown. Here we show that in immature dendritic cells, which patrol their environment by engulfing extracellular material, cell migration and antigen capture are antagonistic. This antagonism results from transient enrichment of myosin IIA at the cell front, which disrupts the back-to-front gradient of the motor protein, slowing down locomotion but promoting antigen capture. We further highlight that myosin IIA enrichment at the cell front requires the MHC class II-associated invariant chain (Ii). Thus, by controlling myosin IIA localization, Ii imposes on dendritic cells an intermittent antigen capture behaviour that might facilitate environment patrolling. We propose that the requirement for myosin II in both cell migration and specific cell functions may provide a general mechanism for their coordination in time and space. acknowledgement: M.C. and M.L.H. were supported by fellowships from the Fondation pour la Recherche Médicale and the Association pour la Recherche contre le Cancer, respectively. This work was funded by grants from the City of Paris and the European Research Council to A.-M.L.-D. (Strapacemi 243103), the Association Nationale pour la Recherche (ANR-09-PIRI-0027-PCVI) and the InnaBiosanté foundation (Micemico) to A.-M.L.-D., M.P. and R.V., and the DCBIOL Labex from the French Government (ANR-10-IDEX-0001-02-PSL* and ANR-11-LABX-0043). The super-resolution SIM microscope was funded through an ERC Advanced Investigator Grant (250367) to Edith Heard (CNRS UMR3215/Inserm U934, Institut Curie). article_number: '7526' author: - first_name: Mélanie full_name: Chabaud, Mélanie last_name: Chabaud - first_name: Mélina full_name: Heuzé, Mélina last_name: Heuzé - first_name: Marine full_name: Bretou, Marine last_name: Bretou - first_name: Pablo full_name: Vargas, Pablo last_name: Vargas - first_name: Paolo full_name: Maiuri, Paolo last_name: Maiuri - first_name: Paola full_name: Solanes, Paola last_name: Solanes - first_name: Mathieu full_name: Maurin, Mathieu last_name: Maurin - first_name: Emmanuel full_name: Terriac, Emmanuel last_name: Terriac - first_name: Maël full_name: Le Berre, Maël last_name: Le Berre - first_name: Danielle full_name: Lankar, Danielle last_name: Lankar - first_name: Tristan full_name: Piolot, Tristan last_name: Piolot - first_name: Robert full_name: Adelstein, Robert last_name: Adelstein - first_name: Yingfan full_name: Zhang, Yingfan last_name: Zhang - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Jordan full_name: Jacobelli, Jordan last_name: Jacobelli - first_name: Olivier full_name: Bénichou, Olivier last_name: Bénichou - first_name: Raphaël full_name: Voituriez, Raphaël last_name: Voituriez - first_name: Matthieu full_name: Piel, Matthieu last_name: Piel - first_name: Ana full_name: Lennon Duménil, Ana last_name: Lennon Duménil citation: ama: Chabaud M, Heuzé M, Bretou M, et al. Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells. Nature Communications. 2015;6. doi:10.1038/ncomms8526 apa: Chabaud, M., Heuzé, M., Bretou, M., Vargas, P., Maiuri, P., Solanes, P., … Lennon Duménil, A. (2015). Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms8526 chicago: Chabaud, Mélanie, Mélina Heuzé, Marine Bretou, Pablo Vargas, Paolo Maiuri, Paola Solanes, Mathieu Maurin, et al. “Cell Migration and Antigen Capture Are Antagonistic Processes Coupled by Myosin II in Dendritic Cells.” Nature Communications. Nature Publishing Group, 2015. https://doi.org/10.1038/ncomms8526. ieee: M. Chabaud et al., “Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells,” Nature Communications, vol. 6. Nature Publishing Group, 2015. ista: Chabaud M, Heuzé M, Bretou M, Vargas P, Maiuri P, Solanes P, Maurin M, Terriac E, Le Berre M, Lankar D, Piolot T, Adelstein R, Zhang Y, Sixt MK, Jacobelli J, Bénichou O, Voituriez R, Piel M, Lennon Duménil A. 2015. Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells. Nature Communications. 6, 7526. mla: Chabaud, Mélanie, et al. “Cell Migration and Antigen Capture Are Antagonistic Processes Coupled by Myosin II in Dendritic Cells.” Nature Communications, vol. 6, 7526, Nature Publishing Group, 2015, doi:10.1038/ncomms8526. short: M. Chabaud, M. Heuzé, M. Bretou, P. Vargas, P. Maiuri, P. Solanes, M. Maurin, E. Terriac, M. Le Berre, D. Lankar, T. Piolot, R. Adelstein, Y. Zhang, M.K. Sixt, J. Jacobelli, O. Bénichou, R. Voituriez, M. Piel, A. Lennon Duménil, Nature Communications 6 (2015). date_created: 2018-12-11T11:52:48Z date_published: 2015-06-25T00:00:00Z date_updated: 2021-01-12T06:51:42Z day: '25' ddc: - '570' department: - _id: MiSi doi: 10.1038/ncomms8526 file: - access_level: open_access checksum: bae12e86be2adb28253f890b8bba8315 content_type: application/pdf creator: system date_created: 2018-12-12T10:11:58Z date_updated: 2020-07-14T12:45:02Z file_id: '4915' file_name: IST-2016-476-v1+1_ncomms8526.pdf file_size: 4530215 relation: main_file file_date_updated: 2020-07-14T12:45:02Z has_accepted_license: '1' intvolume: ' 6' language: - iso: eng month: '06' oa: 1 oa_version: Published Version publication: Nature Communications publication_status: published publisher: Nature Publishing Group publist_id: '5596' pubrep_id: '476' quality_controlled: '1' scopus_import: 1 status: public title: Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 6 year: '2015' ... --- _id: '1676' author: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Erez full_name: Raz, Erez last_name: Raz citation: ama: 'Sixt MK, Raz E. Editorial overview: Cell adhesion and migration. Current Opinion in Cell Biology. 2015;36(10):4-6. doi:10.1016/j.ceb.2015.09.004' apa: 'Sixt, M. K., & Raz, E. (2015). Editorial overview: Cell adhesion and migration. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2015.09.004' chicago: 'Sixt, Michael K, and Erez Raz. “Editorial Overview: Cell Adhesion and Migration.” Current Opinion in Cell Biology. Elsevier, 2015. https://doi.org/10.1016/j.ceb.2015.09.004.' ieee: 'M. K. Sixt and E. Raz, “Editorial overview: Cell adhesion and migration,” Current Opinion in Cell Biology, vol. 36, no. 10. Elsevier, pp. 4–6, 2015.' ista: 'Sixt MK, Raz E. 2015. Editorial overview: Cell adhesion and migration. Current Opinion in Cell Biology. 36(10), 4–6.' mla: 'Sixt, Michael K., and Erez Raz. “Editorial Overview: Cell Adhesion and Migration.” Current Opinion in Cell Biology, vol. 36, no. 10, Elsevier, 2015, pp. 4–6, doi:10.1016/j.ceb.2015.09.004.' short: M.K. Sixt, E. Raz, Current Opinion in Cell Biology 36 (2015) 4–6. date_created: 2018-12-11T11:53:25Z date_published: 2015-10-01T00:00:00Z date_updated: 2021-01-12T06:52:27Z day: '01' department: - _id: MiSi doi: 10.1016/j.ceb.2015.09.004 intvolume: ' 36' issue: '10' language: - iso: eng month: '10' oa_version: None page: 4 - 6 publication: Current Opinion in Cell Biology publication_status: published publisher: Elsevier publist_id: '5473' scopus_import: 1 status: public title: 'Editorial overview: Cell adhesion and migration' type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 36 year: '2015' ... --- _id: '1687' abstract: - lang: eng text: Guided cell movement is essential for development and integrity of animals and crucially involved in cellular immune responses. Leukocytes are professional migratory cells that can navigate through most types of tissues and sense a wide range of directional cues. The responses of these cells to attractants have been mainly explored in tissue culture settings. How leukocytes make directional decisions in situ, within the challenging environment of a tissue maze, is less understood. Here we review recent advances in how leukocytes sense chemical cues in complex tissue settings and make links with paradigms of directed migration in development and Dictyostelium discoideum amoebae. author: - first_name: Milka full_name: Sarris, Milka last_name: Sarris - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Sarris M, Sixt MK. Navigating in tissue mazes: Chemoattractant interpretation in complex environments. Current Opinion in Cell Biology. 2015;36(10):93-102. doi:10.1016/j.ceb.2015.08.001' apa: 'Sarris, M., & Sixt, M. K. (2015). Navigating in tissue mazes: Chemoattractant interpretation in complex environments. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2015.08.001' chicago: 'Sarris, Milka, and Michael K Sixt. “Navigating in Tissue Mazes: Chemoattractant Interpretation in Complex Environments.” Current Opinion in Cell Biology. Elsevier, 2015. https://doi.org/10.1016/j.ceb.2015.08.001.' ieee: 'M. Sarris and M. K. Sixt, “Navigating in tissue mazes: Chemoattractant interpretation in complex environments,” Current Opinion in Cell Biology, vol. 36, no. 10. Elsevier, pp. 93–102, 2015.' ista: 'Sarris M, Sixt MK. 2015. Navigating in tissue mazes: Chemoattractant interpretation in complex environments. Current Opinion in Cell Biology. 36(10), 93–102.' mla: 'Sarris, Milka, and Michael K. Sixt. “Navigating in Tissue Mazes: Chemoattractant Interpretation in Complex Environments.” Current Opinion in Cell Biology, vol. 36, no. 10, Elsevier, 2015, pp. 93–102, doi:10.1016/j.ceb.2015.08.001.' short: M. Sarris, M.K. Sixt, Current Opinion in Cell Biology 36 (2015) 93–102. date_created: 2018-12-11T11:53:28Z date_published: 2015-10-01T00:00:00Z date_updated: 2021-01-12T06:52:31Z day: '01' ddc: - '570' department: - _id: MiSi doi: 10.1016/j.ceb.2015.08.001 ec_funded: 1 file: - access_level: open_access checksum: c29973924b790aab02fdd91857759cfb content_type: application/pdf creator: system date_created: 2018-12-12T10:11:21Z date_updated: 2020-07-14T12:45:12Z file_id: '4875' file_name: IST-2016-445-v1+1_1-s2.0-S0955067415001064-main.pdf file_size: 797964 relation: main_file file_date_updated: 2020-07-14T12:45:12Z has_accepted_license: '1' intvolume: ' 36' issue: '10' language: - iso: eng month: '10' oa: 1 oa_version: Published Version page: 93 - 102 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Current Opinion in Cell Biology publication_status: published publisher: Elsevier publist_id: '5458' pubrep_id: '445' quality_controlled: '1' scopus_import: 1 status: public title: 'Navigating in tissue mazes: Chemoattractant interpretation in complex environments' tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 36 year: '2015' ... --- _id: '1686' author: - first_name: Eva full_name: Kiermaier, Eva id: 3EB04B78-F248-11E8-B48F-1D18A9856A87 last_name: Kiermaier orcid: 0000-0001-6165-5738 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Kiermaier E, Sixt MK. Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. Science. 2015;349(6252):1055-1056. doi:10.1126/science.aad0867' apa: 'Kiermaier, E., & Sixt, M. K. (2015). Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.aad0867' chicago: 'Kiermaier, Eva, and Michael K Sixt. “Fragmented Communication between Immune Cells: Neutrophils Blaze a Trail with Migratory Cues for T Cells to Follow to Sites of Infection.” Science. American Association for the Advancement of Science, 2015. https://doi.org/10.1126/science.aad0867.' ieee: 'E. Kiermaier and M. K. Sixt, “Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection,” Science, vol. 349, no. 6252. American Association for the Advancement of Science, pp. 1055–1056, 2015.' ista: 'Kiermaier E, Sixt MK. 2015. Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. Science. 349(6252), 1055–1056.' mla: 'Kiermaier, Eva, and Michael K. Sixt. “Fragmented Communication between Immune Cells: Neutrophils Blaze a Trail with Migratory Cues for T Cells to Follow to Sites of Infection.” Science, vol. 349, no. 6252, American Association for the Advancement of Science, 2015, pp. 1055–56, doi:10.1126/science.aad0867.' short: E. Kiermaier, M.K. Sixt, Science 349 (2015) 1055–1056. date_created: 2018-12-11T11:53:28Z date_published: 2015-09-04T00:00:00Z date_updated: 2021-01-12T06:52:31Z day: '04' department: - _id: MiSi doi: 10.1126/science.aad0867 intvolume: ' 349' issue: '6252' language: - iso: eng month: '09' oa_version: None page: 1055 - 1056 publication: Science publication_status: published publisher: American Association for the Advancement of Science publist_id: '5459' quality_controlled: '1' scopus_import: 1 status: public title: 'Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection' type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 349 year: '2015' ... --- _id: '477' abstract: - lang: eng text: Dendritic cells are potent antigen-presenting cells endowed with the unique ability to initiate adaptive immune responses upon inflammation. Inflammatory processes are often associated with an increased production of serotonin, which operates by activating specific receptors. However, the functional role of serotonin receptors in regulation of dendritic cell functions is poorly understood. Here, we demonstrate that expression of serotonin receptor 5-HT7 (5-HT7TR) as well as its downstream effector Cdc42 is upregulated in dendritic cells upon maturation. Although dendritic cell maturation was independent of 5-HT7TR, receptor stimulation affected dendritic cell morphology through Cdc42-mediated signaling. In addition, basal activity of 5-HT7TR was required for the proper expression of the chemokine receptor CCR7, which is a key factor that controls dendritic cell migration. Consistent with this, we observed that 5-HT7TR enhances chemotactic motility of dendritic cells in vitro by modulating their directionality and migration velocity. Accordingly, migration of dendritic cells in murine colon explants was abolished after pharmacological receptor inhibition. Our results indicate that there is a crucial role for 5-HT7TR-Cdc42-mediated signaling in the regulation of dendritic cell morphology and motility, suggesting that 5-HT7TR could be a new target for treatment of a variety of inflammatory and immune disorders. author: - first_name: Katrin full_name: Holst, Katrin last_name: Holst - first_name: Daria full_name: Guseva, Daria last_name: Guseva - first_name: Susann full_name: Schindler, Susann last_name: Schindler - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Armin full_name: Braun, Armin last_name: Braun - first_name: Himpriya full_name: Chopra, Himpriya last_name: Chopra - first_name: Oliver full_name: Pabst, Oliver last_name: Pabst - first_name: Evgeni full_name: Ponimaskin, Evgeni last_name: Ponimaskin citation: ama: Holst K, Guseva D, Schindler S, et al. The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. Journal of Cell Science. 2015;128(15):2866-2880. doi:10.1242/jcs.167999 apa: Holst, K., Guseva, D., Schindler, S., Sixt, M. K., Braun, A., Chopra, H., … Ponimaskin, E. (2015). The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.167999 chicago: Holst, Katrin, Daria Guseva, Susann Schindler, Michael K Sixt, Armin Braun, Himpriya Chopra, Oliver Pabst, and Evgeni Ponimaskin. “The Serotonin Receptor 5-HT7R Regulates the Morphology and Migratory Properties of Dendritic Cells.” Journal of Cell Science. Company of Biologists, 2015. https://doi.org/10.1242/jcs.167999. ieee: K. Holst et al., “The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells,” Journal of Cell Science, vol. 128, no. 15. Company of Biologists, pp. 2866–2880, 2015. ista: Holst K, Guseva D, Schindler S, Sixt MK, Braun A, Chopra H, Pabst O, Ponimaskin E. 2015. The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. Journal of Cell Science. 128(15), 2866–2880. mla: Holst, Katrin, et al. “The Serotonin Receptor 5-HT7R Regulates the Morphology and Migratory Properties of Dendritic Cells.” Journal of Cell Science, vol. 128, no. 15, Company of Biologists, 2015, pp. 2866–80, doi:10.1242/jcs.167999. short: K. Holst, D. Guseva, S. Schindler, M.K. Sixt, A. Braun, H. Chopra, O. Pabst, E. Ponimaskin, Journal of Cell Science 128 (2015) 2866–2880. date_created: 2018-12-11T11:46:41Z date_published: 2015-06-15T00:00:00Z date_updated: 2021-01-12T08:00:54Z day: '15' department: - _id: MiSi doi: 10.1242/jcs.167999 intvolume: ' 128' issue: '15' language: - iso: eng month: '06' oa_version: None page: 2866 - 2880 publication: Journal of Cell Science publication_status: published publisher: Company of Biologists publist_id: '7343' quality_controlled: '1' scopus_import: 1 status: public title: The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 128 year: '2015' ...