[{"external_id":{"isi":["000451920600002"]},"abstract":[{"text":"The release of IgM is the first line of an antibody response and precedes the generation of high affinity IgG in germinal centers. Once secreted by freshly activated plasmablasts, IgM is released into the efferent lymph of reactive lymph nodes as early as 3 d after immunization. As pentameric IgM has an enormous size of 1,000 kD, its diffusibility is low, and one might wonder how it can pass through the densely lymphocyte-packed environment of a lymph node parenchyma in order to reach its exit. In this issue of JEM, Thierry et al. show that, in order to reach the blood stream, IgM molecules take a specific micro-anatomical route via lymph node conduits.","lang":"eng"}],"title":"IgM's exit route","doi":"10.1084/jem.20181934","oa_version":"Published Version","language":[{"iso":"eng"}],"date_updated":"2026-04-16T09:54:07Z","publication_status":"published","scopus_import":"1","intvolume":"       215","oa":1,"page":"2959-2961","publication":"Journal of Experimental Medicine","date_created":"2018-12-16T22:59:18Z","ddc":["570"],"isi":1,"month":"11","volume":215,"file_date_updated":"2020-07-14T12:47:09Z","file":[{"relation":"main_file","file_id":"5931","creator":"dernst","content_type":"application/pdf","checksum":"687beea1d64c213f4cb9e3c29ec11a14","file_name":"2018_JournalExperMed_Reversat.pdf","file_size":1216437,"date_created":"2019-02-06T08:49:52Z","date_updated":"2020-07-14T12:47:09Z","access_level":"open_access"}],"license":"https://creativecommons.org/licenses/by-nc-sa/4.0/","status":"public","day":"20","year":"2018","date_published":"2018-11-20T00:00:00Z","department":[{"_id":"MiSi"}],"user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","_id":"5672","article_processing_charge":"No","author":[{"orcid":"0000-0003-0666-8928","id":"35B76592-F248-11E8-B48F-1D18A9856A87","first_name":"Anne","last_name":"Reversat","full_name":"Reversat, Anne"},{"orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","last_name":"Sixt","full_name":"Sixt, Michael K"}],"publisher":"Rockefeller University Press","tmp":{"short":"CC BY-NC-SA (4.0)","image":"/images/cc_by_nc_sa.png","name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode"},"citation":{"apa":"Reversat, A., &#38; Sixt, M. K. (2018). IgM’s exit route. <i>Journal of Experimental Medicine</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1084/jem.20181934\">https://doi.org/10.1084/jem.20181934</a>","ieee":"A. Reversat and M. K. Sixt, “IgM’s exit route,” <i>Journal of Experimental Medicine</i>, vol. 215, no. 12. Rockefeller University Press, pp. 2959–2961, 2018.","short":"A. Reversat, M.K. Sixt, Journal of Experimental Medicine 215 (2018) 2959–2961.","chicago":"Reversat, Anne, and Michael K Sixt. “IgM’s Exit Route.” <i>Journal of Experimental Medicine</i>. Rockefeller University Press, 2018. <a href=\"https://doi.org/10.1084/jem.20181934\">https://doi.org/10.1084/jem.20181934</a>.","ama":"Reversat A, Sixt MK. IgM’s exit route. <i>Journal of Experimental Medicine</i>. 2018;215(12):2959-2961. doi:<a href=\"https://doi.org/10.1084/jem.20181934\">10.1084/jem.20181934</a>","ista":"Reversat A, Sixt MK. 2018. IgM’s exit route. Journal of Experimental Medicine. 215(12), 2959–2961.","mla":"Reversat, Anne, and Michael K. Sixt. “IgM’s Exit Route.” <i>Journal of Experimental Medicine</i>, vol. 215, no. 12, Rockefeller University Press, 2018, pp. 2959–61, doi:<a href=\"https://doi.org/10.1084/jem.20181934\">10.1084/jem.20181934</a>."},"type":"journal_article","quality_controlled":"1","publication_identifier":{"issn":["0022-1007"]},"has_accepted_license":"1","issue":"12"},{"publication_identifier":{"issn":["2663-337X"]},"has_accepted_license":"1","related_material":{"record":[{"id":"1321","relation":"part_of_dissertation","status":"public"}]},"citation":{"mla":"Leithner, Alexander F. <i>Branched Actin Networks in Dendritic Cell Biology</i>. Institute of Science and Technology Austria, 2018, doi:<a href=\"https://doi.org/10.15479/AT:ISTA:th_998\">10.15479/AT:ISTA:th_998</a>.","ieee":"A. F. Leithner, “Branched actin networks in dendritic cell biology,” Institute of Science and Technology Austria, 2018.","apa":"Leithner, A. F. (2018). <i>Branched actin networks in dendritic cell biology</i>. Institute of Science and Technology Austria. <a href=\"https://doi.org/10.15479/AT:ISTA:th_998\">https://doi.org/10.15479/AT:ISTA:th_998</a>","short":"A.F. Leithner, Branched Actin Networks in Dendritic Cell Biology, Institute of Science and Technology Austria, 2018.","chicago":"Leithner, Alexander F. “Branched Actin Networks in Dendritic Cell Biology.” Institute of Science and Technology Austria, 2018. <a href=\"https://doi.org/10.15479/AT:ISTA:th_998\">https://doi.org/10.15479/AT:ISTA:th_998</a>.","ista":"Leithner AF. 2018. Branched actin networks in dendritic cell biology. Institute of Science and Technology Austria.","ama":"Leithner AF. Branched actin networks in dendritic cell biology. 2018. doi:<a href=\"https://doi.org/10.15479/AT:ISTA:th_998\">10.15479/AT:ISTA:th_998</a>"},"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"dissertation","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","department":[{"_id":"MiSi"}],"year":"2018","day":"12","pubrep_id":"998","date_published":"2018-04-12T00:00:00Z","publisher":"Institute of Science and Technology Austria","alternative_title":["ISTA Thesis"],"_id":"323","article_processing_charge":"No","author":[{"full_name":"Leithner, Alexander F","last_name":"Leithner","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander F","orcid":"0000-0002-1073-744X"}],"license":"https://creativecommons.org/licenses/by/4.0/","file":[{"checksum":"d5e3edbac548c26c1fa43a4b37a54a4c","file_name":"PhD_thesis_AlexLeithner_final_version.docx","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","creator":"dernst","file_id":"6219","embargo_to":"open_access","relation":"source_file","access_level":"closed","date_updated":"2021-02-11T23:30:17Z","date_created":"2019-04-05T09:23:11Z","file_size":29027671},{"relation":"main_file","embargo":"2019-04-15","file_id":"6220","creator":"dernst","content_type":"application/pdf","checksum":"071f7476db29e41146824ebd0697cb10","file_name":"PhD_thesis_AlexLeithner.pdf","date_created":"2019-04-05T09:23:11Z","file_size":66045341,"date_updated":"2021-02-11T11:17:16Z","access_level":"open_access"}],"status":"public","file_date_updated":"2021-02-11T23:30:17Z","acknowledgement":"First of all I would like to thank Michael Sixt for giving me the opportunity to work in \r\nhis group and for his support throughout the years. He is a truly inspiring person and \r\nthe  best  boss  one  can  imagine.  I  would  also  like  to  thank  all  current  and  past \r\nmembers of the Sixt group for their help and the great working atmosphere in the lab. \r\nIt is a true privilege to work with such a bright, funny and friendly group of people and \r\nI’m  proud  that  I  could  be  part  of  it.  Furthermore,  I  would  like  to  say  ‘thank  you’  to Daria Siekhaus for all the meetings and discussion we had throughout the years \r\nand to  Federica  Benvenuti  for  being  part  of  my  committee.  I  am  also  grateful  to  Jack \r\nMerrin  in  the  nanofabrication  facility  and  all  the  people  working  in  the  bioimaging-\r\n, the electron microscopy- and the preclinical facilities.","publist_id":"7542","page":"99","date_created":"2018-12-11T11:45:49Z","ddc":["571","599","610"],"month":"04","supervisor":[{"full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"}],"corr_author":"1","oa":1,"oa_version":"Published Version","language":[{"iso":"eng"}],"date_updated":"2025-09-22T08:27:34Z","publication_status":"published","degree_awarded":"PhD","acknowledged_ssus":[{"_id":"NanoFab"},{"_id":"Bio"},{"_id":"PreCl"},{"_id":"EM-Fac"}],"abstract":[{"text":"In the here presented thesis, we explore the role of branched actin networks in cell migration and antigen presentation, the two most relevant processes in dendritic cell biology. Branched actin networks construct lamellipodial protrusions at the leading edge of migrating cells. These are typically seen as adhesive structures, which mediate force transduction to the extracellular matrix that leads to forward locomotion. We ablated Arp2/3 nucleation promoting factor WAVE in DCs and found that the resulting cells lack lamellipodial protrusions. Instead, depending on the maturation state, one or multiple filopodia were formed. By challenging these cells in a variety of migration assays we found that lamellipodial protrusions are dispensable for the locomotion of leukocytes and actually dampen the speed of migration. However, lamellipodia are critically required to negotiate complex environments that DCs experience while they travel to the next draining lymph node. Taken together our results suggest that leukocyte lamellipodia have rather a sensory- than a force transducing function. Furthermore, we show for the first time structure and dynamics of dendritic cell F-actin at the immunological synapse with naïve T cells. Dendritic cell F-actin appears as dynamic foci that are nucleated by the Arp2/3 complex. WAVE ablated dendritic cells show increased membrane tension, leading to an altered ultrastructure of the immunological synapse and severe T cell priming defects. These results point towards a previously unappreciated role of the cellular mechanics of dendritic cells in T cell activation. Additionally, we present a novel cell culture based system for the differentiation of dendritic cells from conditionally immortalized hematopoietic precursors. These precursor cells are genetically tractable via the CRISPR/Cas9 system while they retain their ability to differentiate into highly migratory dendritic cells and other immune cells. This will foster the study of all aspects of dendritic cell biology and beyond. ","lang":"eng"}],"title":"Branched actin networks in dendritic cell biology","doi":"10.15479/AT:ISTA:th_998"},{"status":"public","ec_funded":1,"volume":19,"acknowledgement":"This work was funded by grants from the European Research Council (ERC StG 281556 and CoG 724373) and the Austrian Science Foundation (FWF) to M.S. and by Swiss National Foundation (SNF) project grants 31003A_135649, 31003A_153457 and CR23I3_156234 to J.V.S. F.G. received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 747687, and J.R. was funded by an EMBO long-term fellowship (ALTF 1396-2014).","publist_id":"8040","department":[{"_id":"MiSi"},{"_id":"Bio"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","year":"2018","day":"18","date_published":"2018-05-18T00:00:00Z","publisher":"Nature Publishing Group","article_processing_charge":"No","_id":"15","author":[{"first_name":"Miroslav","id":"4167FE56-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6625-3348","full_name":"Hons, Miroslav","last_name":"Hons"},{"orcid":"0000-0002-2187-6656","first_name":"Aglaja","id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87","last_name":"Kopf","full_name":"Kopf, Aglaja"},{"last_name":"Hauschild","full_name":"Hauschild, Robert","orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","first_name":"Robert"},{"first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-1073-744X","full_name":"Leithner, Alexander F","last_name":"Leithner"},{"last_name":"Gärtner","full_name":"Gärtner, Florian R","orcid":"0000-0001-6120-3723","id":"397A88EE-F248-11E8-B48F-1D18A9856A87","first_name":"Florian R"},{"last_name":"Abe","full_name":"Abe, Jun","first_name":"Jun"},{"orcid":"0000-0003-2856-3369","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","first_name":"Jörg","last_name":"Renkawitz","full_name":"Renkawitz, Jörg"},{"first_name":"Jens","full_name":"Stein, Jens","last_name":"Stein"},{"orcid":"0000-0002-6620-9179","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","full_name":"Sixt, Michael K"}],"citation":{"mla":"Hons, Miroslav, et al. “Chemokines and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal Migration of T Cells.” <i>Nature Immunology</i>, vol. 19, no. 6, Nature Publishing Group, 2018, pp. 606–16, doi:<a href=\"https://doi.org/10.1038/s41590-018-0109-z\">10.1038/s41590-018-0109-z</a>.","ista":"Hons M, Kopf A, Hauschild R, Leithner AF, Gärtner FR, Abe J, Renkawitz J, Stein J, Sixt MK. 2018. Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. Nature Immunology. 19(6), 606–616.","ama":"Hons M, Kopf A, Hauschild R, et al. Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. <i>Nature Immunology</i>. 2018;19(6):606-616. doi:<a href=\"https://doi.org/10.1038/s41590-018-0109-z\">10.1038/s41590-018-0109-z</a>","ieee":"M. Hons <i>et al.</i>, “Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells,” <i>Nature Immunology</i>, vol. 19, no. 6. Nature Publishing Group, pp. 606–616, 2018.","apa":"Hons, M., Kopf, A., Hauschild, R., Leithner, A. F., Gärtner, F. R., Abe, J., … Sixt, M. K. (2018). Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. <i>Nature Immunology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/s41590-018-0109-z\">https://doi.org/10.1038/s41590-018-0109-z</a>","short":"M. Hons, A. Kopf, R. Hauschild, A.F. Leithner, F.R. Gärtner, J. Abe, J. Renkawitz, J. Stein, M.K. Sixt, Nature Immunology 19 (2018) 606–616.","chicago":"Hons, Miroslav, Aglaja Kopf, Robert Hauschild, Alexander F Leithner, Florian R Gärtner, Jun Abe, Jörg Renkawitz, Jens Stein, and Michael K Sixt. “Chemokines and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal Migration of T Cells.” <i>Nature Immunology</i>. Nature Publishing Group, 2018. <a href=\"https://doi.org/10.1038/s41590-018-0109-z\">https://doi.org/10.1038/s41590-018-0109-z</a>."},"type":"journal_article","quality_controlled":"1","project":[{"grant_number":"724373","_id":"25FE9508-B435-11E9-9278-68D0E5697425","name":"Cellular Navigation Along Spatial Gradients","call_identifier":"H2020"},{"grant_number":"747687","call_identifier":"H2020","_id":"260AA4E2-B435-11E9-9278-68D0E5697425","name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells"},{"grant_number":"ALTF 1396-2014","name":"Molecular and system level view of immune cell migration","_id":"25A48D24-B435-11E9-9278-68D0E5697425"},{"_id":"25A603A2-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes","call_identifier":"FP7","grant_number":"281556"}],"pmid":1,"issue":"6","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pubmed/29777221","open_access":"1"}],"related_material":{"record":[{"id":"6891","status":"public","relation":"dissertation_contains"}]},"acknowledged_ssus":[{"_id":"SSU"}],"abstract":[{"text":"Although much is known about the physiological framework of T cell motility, and numerous rate-limiting molecules have been identified through loss-of-function approaches, an integrated functional concept of T cell motility is lacking. Here, we used in vivo precision morphometry together with analysis of cytoskeletal dynamics in vitro to deconstruct the basic mechanisms of T cell migration within lymphatic organs. We show that the contributions of the integrin LFA-1 and the chemokine receptor CCR7 are complementary rather than positioned in a linear pathway, as they are during leukocyte extravasation from the blood vasculature. Our data demonstrate that CCR7 controls cortical actin flows, whereas integrins mediate substrate friction that is sufficient to drive locomotion in the absence of considerable surface adhesions and plasma membrane flux.","lang":"eng"}],"title":"Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells","external_id":{"isi":["000433041500026"],"pmid":["29777221"]},"doi":"10.1038/s41590-018-0109-z","oa_version":"Published Version","language":[{"iso":"eng"}],"scopus_import":"1","publication_status":"published","date_updated":"2026-06-05T22:32:58Z","intvolume":"        19","oa":1,"publication":"Nature Immunology","page":"606 - 616","date_created":"2018-12-11T11:44:10Z","isi":1,"month":"05"},{"citation":{"ista":"Brown M, Assen FP, Leithner AF, Abe J, Schachner H, Asfour G, Bagó Horváth Z, Stein J, Uhrin P, Sixt MK, Kerjaschki D. 2018. Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. Science. 359(6382), 1408–1411.","ama":"Brown M, Assen FP, Leithner AF, et al. Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. <i>Science</i>. 2018;359(6382):1408-1411. doi:<a href=\"https://doi.org/10.1126/science.aal3662\">10.1126/science.aal3662</a>","chicago":"Brown, Markus, Frank P Assen, Alexander F Leithner, Jun Abe, Helga Schachner, Gabriele Asfour, Zsuzsanna Bagó Horváth, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” <i>Science</i>. American Association for the Advancement of Science, 2018. <a href=\"https://doi.org/10.1126/science.aal3662\">https://doi.org/10.1126/science.aal3662</a>.","short":"M. Brown, F.P. Assen, A.F. Leithner, J. Abe, H. Schachner, G. Asfour, Z. Bagó Horváth, J. Stein, P. Uhrin, M.K. Sixt, D. Kerjaschki, Science 359 (2018) 1408–1411.","apa":"Brown, M., Assen, F. P., Leithner, A. F., Abe, J., Schachner, H., Asfour, G., … Kerjaschki, D. (2018). Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.aal3662\">https://doi.org/10.1126/science.aal3662</a>","ieee":"M. Brown <i>et al.</i>, “Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice,” <i>Science</i>, vol. 359, no. 6382. American Association for the Advancement of Science, pp. 1408–1411, 2018.","mla":"Brown, Markus, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” <i>Science</i>, vol. 359, no. 6382, American Association for the Advancement of Science, 2018, pp. 1408–11, doi:<a href=\"https://doi.org/10.1126/science.aal3662\">10.1126/science.aal3662</a>."},"article_type":"original","project":[{"name":"Cytoskeletal force generation and force transduction of migrating leukocytes","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"Y 564-B12"},{"name":"Cytoskeletal force generation and force transduction of migrating leukocytes","_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","grant_number":"281556"}],"quality_controlled":"1","type":"journal_article","pmid":1,"main_file_link":[{"open_access":"1","url":"https://doi.org/10.1126/science.aal3662"}],"issue":"6382","related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"6947"}]},"ec_funded":1,"status":"public","volume":359,"acknowledgement":"M.B. was supported by the Cell Communication in Health and Disease graduate study program of the Austrian Science Fund (FWF) and the Medical University of Vienna. M.S. was supported by the European Research Council (grant ERC GA 281556) and an FWF START award.\r\nWe thank C. Moussion for establishing the intralymphatic injection at IST Austria and for providing anti-PNAd hybridoma supernatant, R. Förster and A. Braun for sharing the intralymphatic injection technology, K. Vaahtomeri for the lentiviral constructs, M. Hons for establishing in vivo multiphoton imaging, the Sixt lab for intellectual input, M. Schunn for help with the design of the in vivo experiments, F. Langer for technical assistance with the in vivo experiments, the bioimaging facility of IST Austria for support, and R. Efferl for providing the CT26 cell line.","publist_id":"7428","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","department":[{"_id":"MiSi"}],"date_published":"2018-03-23T00:00:00Z","year":"2018","day":"23","publisher":"American Association for the Advancement of Science","article_processing_charge":"No","_id":"402","author":[{"last_name":"Brown","full_name":"Brown, Markus","first_name":"Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Assen, Frank P","last_name":"Assen","first_name":"Frank P","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-3470-6119"},{"id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander F","orcid":"0000-0002-1073-744X","full_name":"Leithner, Alexander F","last_name":"Leithner"},{"full_name":"Abe, Jun","last_name":"Abe","first_name":"Jun"},{"last_name":"Schachner","full_name":"Schachner, Helga","first_name":"Helga"},{"last_name":"Asfour","full_name":"Asfour, Gabriele","first_name":"Gabriele"},{"last_name":"Bagó Horváth","full_name":"Bagó Horváth, Zsuzsanna","first_name":"Zsuzsanna"},{"first_name":"Jens","full_name":"Stein, Jens","last_name":"Stein"},{"last_name":"Uhrin","full_name":"Uhrin, Pavel","first_name":"Pavel"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Kerjaschki, Dontscho","last_name":"Kerjaschki","first_name":"Dontscho"}],"intvolume":"       359","oa":1,"date_created":"2018-12-11T11:46:16Z","page":"1408 - 1411","publication":"Science","month":"03","isi":1,"corr_author":"1","title":"Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice","acknowledged_ssus":[{"_id":"Bio"}],"abstract":[{"lang":"eng","text":"During metastasis, malignant cells escape the primary tumor, intravasate lymphatic vessels, and reach draining sentinel lymph nodes before they colonize distant organs via the blood circulation. Although lymph node metastasis in cancer patients correlates with poor prognosis, evidence is lacking as to whether and how tumor cells enter the bloodstream via lymph nodes. To investigate this question, we delivered carcinoma cells into the lymph nodes of mice by microinfusing the cells into afferent lymphatic vessels. We found that tumor cells rapidly infiltrated the lymph node parenchyma, invaded blood vessels, and seeded lung metastases without involvement of the thoracic duct. These results suggest that the lymph node blood vessels can serve as an exit route for systemic dissemination of cancer cells in experimental mouse models. Whether this form of tumor cell spreading occurs in cancer patients remains to be determined."}],"external_id":{"isi":["000428043600047"],"pmid":["29567714"]},"doi":"10.1126/science.aal3662","language":[{"iso":"eng"}],"oa_version":"Published Version","scopus_import":"1","date_updated":"2026-06-05T22:34:18Z","publication_status":"published"},{"date_created":"2018-12-11T11:50:29Z","page":"R24 - R25","publication":"Current Biology","month":"01","isi":1,"intvolume":"        27","oa":1,"language":[{"iso":"eng"}],"oa_version":"Published Version","date_updated":"2025-06-26T09:01:10Z","publication_status":"published","scopus_import":"1","external_id":{"isi":["000391902500010"]},"abstract":[{"text":"Coordinated changes of cell shape are often the result of the excitable, wave-like dynamics of the actin cytoskeleton. New work shows that, in migrating cells, protrusion waves arise from mechanochemical crosstalk between adhesion sites, membrane tension and the actin protrusive machinery.","lang":"eng"}],"title":"Cell migration: Making the waves","OA_place":"publisher","doi":"10.1016/j.cub.2016.11.035","publication_identifier":{"issn":["09609822"]},"issue":"1","main_file_link":[{"url":"https://doi.org/10.1016/j.cub.2016.11.035","open_access":"1"}],"OA_type":"free access","article_type":"letter_note","citation":{"short":"J. Müller, M.K. Sixt, Current Biology 27 (2017) R24–R25.","chicago":"Müller, Jan, and Michael K Sixt. “Cell Migration: Making the Waves.” <i>Current Biology</i>. Cell Press, 2017. <a href=\"https://doi.org/10.1016/j.cub.2016.11.035\">https://doi.org/10.1016/j.cub.2016.11.035</a>.","ieee":"J. Müller and M. K. Sixt, “Cell migration: Making the waves,” <i>Current Biology</i>, vol. 27, no. 1. Cell Press, pp. R24–R25, 2017.","apa":"Müller, J., &#38; Sixt, M. K. (2017). Cell migration: Making the waves. <i>Current Biology</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.cub.2016.11.035\">https://doi.org/10.1016/j.cub.2016.11.035</a>","ista":"Müller J, Sixt MK. 2017. Cell migration: Making the waves. Current Biology. 27(1), R24–R25.","ama":"Müller J, Sixt MK. Cell migration: Making the waves. <i>Current Biology</i>. 2017;27(1):R24-R25. doi:<a href=\"https://doi.org/10.1016/j.cub.2016.11.035\">10.1016/j.cub.2016.11.035</a>","mla":"Müller, Jan, and Michael K. Sixt. “Cell Migration: Making the Waves.” <i>Current Biology</i>, vol. 27, no. 1, Cell Press, 2017, pp. R24–25, doi:<a href=\"https://doi.org/10.1016/j.cub.2016.11.035\">10.1016/j.cub.2016.11.035</a>."},"quality_controlled":"1","type":"journal_article","date_published":"2017-01-09T00:00:00Z","year":"2017","day":"09","department":[{"_id":"MiSi"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"1161","article_processing_charge":"No","author":[{"id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D","first_name":"Jan","last_name":"Müller","full_name":"Müller, Jan"},{"full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"}],"publisher":"Cell Press","volume":27,"status":"public","publist_id":"6197"},{"publisher":"Institute of Science and Technology Austria","article_processing_charge":"No","_id":"5567","date_updated":"2024-02-21T13:47:00Z","author":[{"first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-1073-744X","full_name":"Leithner, Alexander F","last_name":"Leithner"}],"department":[{"_id":"MiSi"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","oa_version":"Published Version","year":"2017","day":"09","date_published":"2017-08-09T00:00:00Z","doi":"10.15479/AT:ISTA:71","file":[{"creator":"system","checksum":"3d6942d47d0737d064706b5728c4d8c8","content_type":"video/x-msvideo","file_name":"IST-2017-71-v1+1_Synapse_1.avi","relation":"main_file","file_id":"5612","date_updated":"2020-07-14T12:47:04Z","access_level":"open_access","date_created":"2018-12-12T13:02:47Z","file_size":236204020},{"access_level":"open_access","date_updated":"2020-07-14T12:47:04Z","date_created":"2018-12-12T13:02:51Z","file_size":226232496,"content_type":"video/x-msvideo","checksum":"4850006c047b0147a9e85b3c2f6f0af4","file_name":"IST-2017-71-v1+2_Synapse_2.avi","creator":"system","file_id":"5613","relation":"main_file"}],"license":"https://creativecommons.org/publicdomain/zero/1.0/","abstract":[{"text":"Immunological synapse DC-Tcells","lang":"eng"}],"status":"public","title":"Immunological synapse DC-Tcells","file_date_updated":"2020-07-14T12:47:04Z","ddc":["570"],"month":"08","keyword":["Immunological synapse"],"has_accepted_license":"1","date_created":"2018-12-12T12:31:34Z","datarep_id":"71","oa":1,"type":"research_data","citation":{"mla":"Leithner, Alexander F. <i>Immunological Synapse DC-Tcells</i>. Institute of Science and Technology Austria, 2017, doi:<a href=\"https://doi.org/10.15479/AT:ISTA:71\">10.15479/AT:ISTA:71</a>.","ieee":"A. F. Leithner, “Immunological synapse DC-Tcells.” Institute of Science and Technology Austria, 2017.","apa":"Leithner, A. F. (2017). Immunological synapse DC-Tcells. Institute of Science and Technology Austria. <a href=\"https://doi.org/10.15479/AT:ISTA:71\">https://doi.org/10.15479/AT:ISTA:71</a>","short":"A.F. Leithner, (2017).","chicago":"Leithner, Alexander F. “Immunological Synapse DC-Tcells.” Institute of Science and Technology Austria, 2017. <a href=\"https://doi.org/10.15479/AT:ISTA:71\">https://doi.org/10.15479/AT:ISTA:71</a>.","ista":"Leithner AF. 2017. Immunological synapse DC-Tcells, Institute of Science and Technology Austria, <a href=\"https://doi.org/10.15479/AT:ISTA:71\">10.15479/AT:ISTA:71</a>.","ama":"Leithner AF. Immunological synapse DC-Tcells. 2017. doi:<a href=\"https://doi.org/10.15479/AT:ISTA:71\">10.15479/AT:ISTA:71</a>"},"tmp":{"short":"CC0 (1.0)","legal_code_url":"https://creativecommons.org/publicdomain/zero/1.0/legalcode","image":"/images/cc_0.png","name":"Creative Commons Public Domain Dedication (CC0 1.0)"}},{"publication_status":"published","date_updated":"2025-09-11T07:41:10Z","scopus_import":"1","language":[{"iso":"eng"}],"oa_version":"Published Version","doi":"10.7554/eLife.30867","external_id":{"isi":["000414407700001"]},"title":"Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments","abstract":[{"text":"The actomyosin ring generates force to ingress the cytokinetic cleavage furrow in animal cells, yet its filament organization and the mechanism of contractility is not well understood. We quantified actin filament order in human cells using fluorescence polarization microscopy and found that cleavage furrow ingression initiates by contraction of an equatorial actin network with randomly oriented filaments. The network subsequently gradually reoriented actin filaments along the cell equator. This strictly depended on myosin II activity, suggesting local network reorganization by mechanical forces. Cortical laser microsurgery revealed that during cytokinesis progression, mechanical tension increased substantially along the direction of the cell equator, while the network contracted laterally along the pole-to-pole axis without a detectable increase in tension. Our data suggest that an asymmetric increase in cortical tension promotes filament reorientation along the cytokinetic cleavage furrow, which might have implications for diverse other biological processes involving actomyosin rings.","lang":"eng"}],"month":"11","isi":1,"ddc":["570"],"date_created":"2018-12-11T11:47:14Z","publication":"eLife","oa":1,"intvolume":"         6","_id":"569","author":[{"first_name":"Felix","full_name":"Spira, Felix","last_name":"Spira"},{"first_name":"Sara","last_name":"Cuylen Haering","full_name":"Cuylen Haering, Sara"},{"last_name":"Mehta","full_name":"Mehta, Shalin","first_name":"Shalin"},{"last_name":"Samwer","full_name":"Samwer, Matthias","first_name":"Matthias"},{"orcid":"0000-0003-0666-8928","id":"35B76592-F248-11E8-B48F-1D18A9856A87","first_name":"Anne","last_name":"Reversat","full_name":"Reversat, Anne"},{"last_name":"Verma","full_name":"Verma, Amitabh","first_name":"Amitabh"},{"full_name":"Oldenbourg, Rudolf","last_name":"Oldenbourg","first_name":"Rudolf"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt"},{"full_name":"Gerlich, Daniel","last_name":"Gerlich","first_name":"Daniel"}],"article_processing_charge":"No","publisher":"eLife Sciences Publications","date_published":"2017-11-06T00:00:00Z","pubrep_id":"919","year":"2017","day":"06","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","department":[{"_id":"MiSi"}],"publist_id":"7245","volume":6,"file_date_updated":"2020-07-14T12:47:10Z","status":"public","file":[{"date_created":"2018-12-12T10:10:40Z","file_size":9666973,"date_updated":"2020-07-14T12:47:10Z","access_level":"open_access","relation":"main_file","file_id":"4829","creator":"system","file_name":"IST-2017-919-v1+1_elife-30867-figures-v1.pdf","checksum":"ba09c1451153d39e4f4b7cee013e314c","content_type":"application/pdf"},{"content_type":"application/pdf","checksum":"01eb51f1d6ad679947415a51c988e137","file_name":"IST-2017-919-v1+2_elife-30867-v1.pdf","creator":"system","file_id":"4830","relation":"main_file","access_level":"open_access","date_updated":"2020-07-14T12:47:10Z","file_size":5951246,"date_created":"2018-12-12T10:10:41Z"}],"article_number":"e30867","has_accepted_license":"1","publication_identifier":{"issn":["2050-084X"]},"quality_controlled":"1","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"citation":{"mla":"Spira, Felix, et al. “Cytokinesis in Vertebrate Cells Initiates by Contraction of an Equatorial Actomyosin Network Composed of Randomly Oriented Filaments.” <i>ELife</i>, vol. 6, e30867, eLife Sciences Publications, 2017, doi:<a href=\"https://doi.org/10.7554/eLife.30867\">10.7554/eLife.30867</a>.","apa":"Spira, F., Cuylen Haering, S., Mehta, S., Samwer, M., Reversat, A., Verma, A., … Gerlich, D. (2017). Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/eLife.30867\">https://doi.org/10.7554/eLife.30867</a>","ieee":"F. Spira <i>et al.</i>, “Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments,” <i>eLife</i>, vol. 6. eLife Sciences Publications, 2017.","short":"F. Spira, S. Cuylen Haering, S. Mehta, M. Samwer, A. Reversat, A. Verma, R. Oldenbourg, M.K. Sixt, D. Gerlich, ELife 6 (2017).","chicago":"Spira, Felix, Sara Cuylen Haering, Shalin Mehta, Matthias Samwer, Anne Reversat, Amitabh Verma, Rudolf Oldenbourg, Michael K Sixt, and Daniel Gerlich. “Cytokinesis in Vertebrate Cells Initiates by Contraction of an Equatorial Actomyosin Network Composed of Randomly Oriented Filaments.” <i>ELife</i>. eLife Sciences Publications, 2017. <a href=\"https://doi.org/10.7554/eLife.30867\">https://doi.org/10.7554/eLife.30867</a>.","ista":"Spira F, Cuylen Haering S, Mehta S, Samwer M, Reversat A, Verma A, Oldenbourg R, Sixt MK, Gerlich D. 2017. Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. eLife. 6, e30867.","ama":"Spira F, Cuylen Haering S, Mehta S, et al. Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. <i>eLife</i>. 2017;6. doi:<a href=\"https://doi.org/10.7554/eLife.30867\">10.7554/eLife.30867</a>"}},{"external_id":{"isi":["000417362700018"]},"title":"Migrating platelets are mechano scavengers that collect and bundle bacteria","abstract":[{"lang":"eng","text":"Blood platelets are critical for hemostasis and thrombosis and play diverse roles during immune responses. Despite these versatile tasks in mammalian biology, their skills on a cellular level are deemed limited, mainly consisting in rolling, adhesion, and aggregate formation. Here, we identify an unappreciated asset of platelets and show that adherent platelets use adhesion receptors to mechanically probe the adhesive substrate in their local microenvironment. When actomyosin-dependent traction forces overcome substrate resistance, platelets migrate and pile up the adhesive substrate together with any bound particulate material. They use this ability to act as cellular scavengers, scanning the vascular surface for potential invaders and collecting deposited bacteria. Microbe collection by migrating platelets boosts the activity of professional phagocytes, exacerbating inflammatory tissue injury in sepsis. This assigns platelets a central role in innate immune responses and identifies them as potential targets to dampen inflammatory tissue damage in clinical scenarios of severe systemic infection. In addition to their role in thrombosis and hemostasis, platelets can also migrate to sites of infection to help trap bacteria and clear the vascular surface."}],"doi":"10.1016/j.cell.2017.11.001","language":[{"iso":"eng"}],"oa_version":"None","publication_status":"published","date_updated":"2025-09-11T07:39:45Z","scopus_import":"1","intvolume":"       171","date_created":"2018-12-11T11:47:15Z","publication":"Cell Press","page":"1368 - 1382","month":"11","isi":1,"volume":171,"status":"public","ec_funded":1,"publist_id":"7243","date_published":"2017-11-30T00:00:00Z","year":"2017","day":"30","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","department":[{"_id":"MiSi"}],"_id":"571","article_processing_charge":"No","author":[{"full_name":"Gärtner, Florian R","last_name":"Gärtner","first_name":"Florian R","id":"397A88EE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6120-3723"},{"last_name":"Ahmad","full_name":"Ahmad, Zerkah","first_name":"Zerkah"},{"first_name":"Gerhild","last_name":"Rosenberger","full_name":"Rosenberger, Gerhild"},{"first_name":"Shuxia","full_name":"Fan, Shuxia","last_name":"Fan"},{"first_name":"Leo","last_name":"Nicolai","full_name":"Nicolai, Leo"},{"full_name":"Busch, Benjamin","last_name":"Busch","first_name":"Benjamin"},{"first_name":"Gökce","last_name":"Yavuz","full_name":"Yavuz, Gökce"},{"first_name":"Manja","full_name":"Luckner, Manja","last_name":"Luckner"},{"full_name":"Ishikawa Ankerhold, Hellen","last_name":"Ishikawa Ankerhold","first_name":"Hellen"},{"first_name":"Roman","full_name":"Hennel, Roman","last_name":"Hennel"},{"first_name":"Alexandre","full_name":"Benechet, Alexandre","last_name":"Benechet"},{"first_name":"Michael","full_name":"Lorenz, Michael","last_name":"Lorenz"},{"first_name":"Sue","last_name":"Chandraratne","full_name":"Chandraratne, Sue"},{"first_name":"Irene","full_name":"Schubert, Irene","last_name":"Schubert"},{"full_name":"Helmer, Sebastian","last_name":"Helmer","first_name":"Sebastian"},{"first_name":"Bianca","last_name":"Striednig","full_name":"Striednig, Bianca"},{"first_name":"Konstantin","last_name":"Stark","full_name":"Stark, Konstantin"},{"first_name":"Marek","last_name":"Janko","full_name":"Janko, Marek"},{"last_name":"Böttcher","full_name":"Böttcher, Ralph","first_name":"Ralph"},{"first_name":"Admar","full_name":"Verschoor, Admar","last_name":"Verschoor"},{"last_name":"Leon","full_name":"Leon, Catherine","first_name":"Catherine"},{"full_name":"Gachet, Christian","last_name":"Gachet","first_name":"Christian"},{"first_name":"Thomas","full_name":"Gudermann, Thomas","last_name":"Gudermann"},{"full_name":"Mederos Y Schnitzler, Michael","last_name":"Mederos Y Schnitzler","first_name":"Michael"},{"first_name":"Zachary","last_name":"Pincus","full_name":"Pincus, Zachary"},{"first_name":"Matteo","last_name":"Iannacone","full_name":"Iannacone, Matteo"},{"last_name":"Haas","full_name":"Haas, Rainer","first_name":"Rainer"},{"first_name":"Gerhard","last_name":"Wanner","full_name":"Wanner, Gerhard"},{"first_name":"Kirsten","last_name":"Lauber","full_name":"Lauber, Kirsten"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt"},{"full_name":"Massberg, Steffen","last_name":"Massberg","first_name":"Steffen"}],"publisher":"Cell Press","citation":{"mla":"Gärtner, Florian R., et al. “Migrating Platelets Are Mechano Scavengers That Collect and Bundle Bacteria.” <i>Cell Press</i>, vol. 171, no. 6, Cell Press, 2017, pp. 1368–82, doi:<a href=\"https://doi.org/10.1016/j.cell.2017.11.001\">10.1016/j.cell.2017.11.001</a>.","apa":"Gärtner, F. R., Ahmad, Z., Rosenberger, G., Fan, S., Nicolai, L., Busch, B., … Massberg, S. (2017). Migrating platelets are mechano scavengers that collect and bundle bacteria. <i>Cell Press</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.cell.2017.11.001\">https://doi.org/10.1016/j.cell.2017.11.001</a>","ieee":"F. R. Gärtner <i>et al.</i>, “Migrating platelets are mechano scavengers that collect and bundle bacteria,” <i>Cell Press</i>, vol. 171, no. 6. Cell Press, pp. 1368–1382, 2017.","short":"F.R. Gärtner, Z. Ahmad, G. Rosenberger, S. Fan, L. Nicolai, B. Busch, G. Yavuz, M. Luckner, H. Ishikawa Ankerhold, R. Hennel, A. Benechet, M. Lorenz, S. Chandraratne, I. Schubert, S. Helmer, B. Striednig, K. Stark, M. Janko, R. Böttcher, A. Verschoor, C. Leon, C. Gachet, T. Gudermann, M. Mederos Y Schnitzler, Z. Pincus, M. Iannacone, R. Haas, G. Wanner, K. Lauber, M.K. Sixt, S. Massberg, Cell Press 171 (2017) 1368–1382.","chicago":"Gärtner, Florian R, Zerkah Ahmad, Gerhild Rosenberger, Shuxia Fan, Leo Nicolai, Benjamin Busch, Gökce Yavuz, et al. “Migrating Platelets Are Mechano Scavengers That Collect and Bundle Bacteria.” <i>Cell Press</i>. Cell Press, 2017. <a href=\"https://doi.org/10.1016/j.cell.2017.11.001\">https://doi.org/10.1016/j.cell.2017.11.001</a>.","ama":"Gärtner FR, Ahmad Z, Rosenberger G, et al. Migrating platelets are mechano scavengers that collect and bundle bacteria. <i>Cell Press</i>. 2017;171(6):1368-1382. doi:<a href=\"https://doi.org/10.1016/j.cell.2017.11.001\">10.1016/j.cell.2017.11.001</a>","ista":"Gärtner FR, Ahmad Z, Rosenberger G, Fan S, Nicolai L, Busch B, Yavuz G, Luckner M, Ishikawa Ankerhold H, Hennel R, Benechet A, Lorenz M, Chandraratne S, Schubert I, Helmer S, Striednig B, Stark K, Janko M, Böttcher R, Verschoor A, Leon C, Gachet C, Gudermann T, Mederos Y Schnitzler M, Pincus Z, Iannacone M, Haas R, Wanner G, Lauber K, Sixt MK, Massberg S. 2017. Migrating platelets are mechano scavengers that collect and bundle bacteria. Cell Press. 171(6), 1368–1382."},"quality_controlled":"1","project":[{"name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells","_id":"260AA4E2-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"747687"}],"type":"journal_article","publication_identifier":{"issn":["0092-8674"]},"issue":"6"},{"publication_status":"published","date_updated":"2025-09-11T07:09:28Z","scopus_import":"1","language":[{"iso":"eng"}],"oa_version":"Published Version","doi":"10.1038/ncomms14832","external_id":{"isi":["000396993700001"]},"title":"FMNL formins boost lamellipodial force generation","abstract":[{"text":"Migration frequently involves Rac-mediated protrusion of lamellipodia, formed by Arp2/3 complex-dependent branching thought to be crucial for force generation and stability of these networks. The formins FMNL2 and FMNL3 are Cdc42 effectors targeting to the lamellipodium tip and shown here to nucleate and elongate actin filaments with complementary activities in vitro. In migrating B16-F1 melanoma cells, both formins contribute to the velocity of lamellipodium protrusion. Loss of FMNL2/3 function in melanoma cells and fibroblasts reduces lamellipodial width, actin filament density and -bundling, without changing patterns of Arp2/3 complex incorporation. Strikingly, in melanoma cells, FMNL2/3 gene inactivation almost completely abolishes protrusion forces exerted by lamellipodia and modifies their ultrastructural organization. Consistently, CRISPR/Cas-mediated depletion of FMNL2/3 in fibroblasts reduces both migration and capability of cells to move against viscous media. Together, we conclude that force generation in lamellipodia strongly depends on FMNL formin activity, operating in addition to Arp2/3 complex-dependent filament branching.","lang":"eng"}],"month":"03","isi":1,"ddc":["570"],"date_created":"2018-12-11T11:47:46Z","publication":"Nature Communications","oa":1,"intvolume":"         8","author":[{"first_name":"Frieda","last_name":"Kage","full_name":"Kage, Frieda"},{"first_name":"Moritz","full_name":"Winterhoff, Moritz","last_name":"Winterhoff"},{"full_name":"Dimchev, Vanessa","last_name":"Dimchev","first_name":"Vanessa"},{"last_name":"Müller","full_name":"Müller, Jan","first_name":"Jan","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D"},{"full_name":"Thalheim, Tobias","last_name":"Thalheim","first_name":"Tobias"},{"full_name":"Freise, Anika","last_name":"Freise","first_name":"Anika"},{"full_name":"Brühmann, Stefan","last_name":"Brühmann","first_name":"Stefan"},{"last_name":"Kollasser","full_name":"Kollasser, Jana","first_name":"Jana"},{"last_name":"Block","full_name":"Block, Jennifer","first_name":"Jennifer"},{"full_name":"Dimchev, Georgi A","last_name":"Dimchev","first_name":"Georgi A"},{"full_name":"Geyer, Matthias","last_name":"Geyer","first_name":"Matthias"},{"first_name":"Hams","full_name":"Schnittler, Hams","last_name":"Schnittler"},{"first_name":"Cord","last_name":"Brakebusch","full_name":"Brakebusch, Cord"},{"first_name":"Theresia","last_name":"Stradal","full_name":"Stradal, Theresia"},{"last_name":"Carlier","full_name":"Carlier, Marie","first_name":"Marie"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"},{"first_name":"Josef","full_name":"Käs, Josef","last_name":"Käs"},{"last_name":"Faix","full_name":"Faix, Jan","first_name":"Jan"},{"last_name":"Rottner","full_name":"Rottner, Klemens","first_name":"Klemens"}],"_id":"659","article_processing_charge":"No","publisher":"Nature Publishing Group","pubrep_id":"902","date_published":"2017-03-22T00:00:00Z","day":"22","year":"2017","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","department":[{"_id":"MiSi"}],"publist_id":"7075","file_date_updated":"2020-07-14T12:47:34Z","volume":8,"status":"public","file":[{"file_id":"5072","relation":"main_file","content_type":"application/pdf","checksum":"dae30190291c3630e8102d8714a8d23e","file_name":"IST-2017-902-v1+1_Kage_et_al-2017-Nature_Communications.pdf","creator":"system","file_size":9523746,"date_created":"2018-12-12T10:14:21Z","access_level":"open_access","date_updated":"2020-07-14T12:47:34Z"}],"article_number":"14832","has_accepted_license":"1","publication_identifier":{"issn":["2041-1723"]},"quality_controlled":"1","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"citation":{"mla":"Kage, Frieda, et al. “FMNL Formins Boost Lamellipodial Force Generation.” <i>Nature Communications</i>, vol. 8, 14832, Nature Publishing Group, 2017, doi:<a href=\"https://doi.org/10.1038/ncomms14832\">10.1038/ncomms14832</a>.","short":"F. Kage, M. Winterhoff, V. Dimchev, J. Müller, T. Thalheim, A. Freise, S. Brühmann, J. Kollasser, J. Block, G.A. Dimchev, M. Geyer, H. Schnittler, C. Brakebusch, T. Stradal, M. Carlier, M.K. Sixt, J. Käs, J. Faix, K. Rottner, Nature Communications 8 (2017).","chicago":"Kage, Frieda, Moritz Winterhoff, Vanessa Dimchev, Jan Müller, Tobias Thalheim, Anika Freise, Stefan Brühmann, et al. “FMNL Formins Boost Lamellipodial Force Generation.” <i>Nature Communications</i>. Nature Publishing Group, 2017. <a href=\"https://doi.org/10.1038/ncomms14832\">https://doi.org/10.1038/ncomms14832</a>.","apa":"Kage, F., Winterhoff, M., Dimchev, V., Müller, J., Thalheim, T., Freise, A., … Rottner, K. (2017). FMNL formins boost lamellipodial force generation. <i>Nature Communications</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/ncomms14832\">https://doi.org/10.1038/ncomms14832</a>","ieee":"F. Kage <i>et al.</i>, “FMNL formins boost lamellipodial force generation,” <i>Nature Communications</i>, vol. 8. Nature Publishing Group, 2017.","ama":"Kage F, Winterhoff M, Dimchev V, et al. FMNL formins boost lamellipodial force generation. <i>Nature Communications</i>. 2017;8. doi:<a href=\"https://doi.org/10.1038/ncomms14832\">10.1038/ncomms14832</a>","ista":"Kage F, Winterhoff M, Dimchev V, Müller J, Thalheim T, Freise A, Brühmann S, Kollasser J, Block J, Dimchev GA, Geyer M, Schnittler H, Brakebusch C, Stradal T, Carlier M, Sixt MK, Käs J, Faix J, Rottner K. 2017. FMNL formins boost lamellipodial force generation. Nature Communications. 8, 14832."}},{"month":"04","ddc":["570"],"isi":1,"date_created":"2018-12-11T11:47:49Z","publication":"Journal of Biological Chemistry","page":"7258 - 7273","oa":1,"intvolume":"       292","scopus_import":"1","date_updated":"2025-09-11T07:03:17Z","publication_status":"published","language":[{"iso":"eng"}],"oa_version":"Published Version","doi":"10.1074/jbc.M116.766923","title":"Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion","abstract":[{"text":"Macrophage filopodia, finger-like membrane protrusions, were first implicated in phagocytosis more than 100 years ago, but little is still known about the involvement of these actin-dependent structures in particle clearance. Using spinning disk confocal microscopy to image filopodial dynamics in mouse resident Lifeact-EGFP macrophages, we show that filopodia, or filopodia-like structures, support pathogen clearance by multiple means. Filopodia supported the phagocytic uptake of bacterial (Escherichia coli) particles by (i) capturing along the filopodial shaft and surfing toward the cell body, the most common mode of capture; (ii) capturing via the tip followed by retraction; (iii) combinations of surfing and retraction; or (iv) sweeping actions. In addition, filopodia supported the uptake of zymosan (Saccharomyces cerevisiae) particles by (i) providing fixation, (ii) capturing at the tip and filopodia-guided actin anterograde flow with phagocytic cup formation, and (iii) the rapid growth of new protrusions. To explore the role of filopodia-inducing Cdc42, we generated myeloid-restricted Cdc42 knock-out mice. Cdc42-deficient macrophages exhibited rapid phagocytic cup kinetics, but reduced particle clearance, which could be explained by the marked rounded-up morphology of these cells. Macrophages lacking Myo10, thought to act downstream of Cdc42, had normal morphology, motility, and phagocytic cup formation, but displayed markedly reduced filopodia formation. In conclusion, live-cell imaging revealed multiple mechanisms involving macrophage filopodia in particle capture and engulfment. Cdc42 is not critical for filopodia or phagocytic cup formation, but plays a key role in driving macrophage lamellipodial spreading.","lang":"eng"}],"external_id":{"isi":["000400478300035"]},"issue":"17","has_accepted_license":"1","publication_identifier":{"issn":["0021-9258"]},"quality_controlled":"1","type":"journal_article","citation":{"mla":"Horsthemke, Markus, et al. “Multiple Roles of Filopodial Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” <i>Journal of Biological Chemistry</i>, vol. 292, no. 17, American Society for Biochemistry and Molecular Biology, 2017, pp. 7258–73, doi:<a href=\"https://doi.org/10.1074/jbc.M116.766923\">10.1074/jbc.M116.766923</a>.","chicago":"Horsthemke, Markus, Anne Bachg, Katharina Groll, Sven Moyzio, Barbara Müther, Sandra Hemkemeyer, Roland Wedlich Söldner, et al. “Multiple Roles of Filopodial Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” <i>Journal of Biological Chemistry</i>. American Society for Biochemistry and Molecular Biology, 2017. <a href=\"https://doi.org/10.1074/jbc.M116.766923\">https://doi.org/10.1074/jbc.M116.766923</a>.","short":"M. Horsthemke, A. Bachg, K. Groll, S. Moyzio, B. Müther, S. Hemkemeyer, R. Wedlich Söldner, M.K. Sixt, S. Tacke, M. Bähler, P. Hanley, Journal of Biological Chemistry 292 (2017) 7258–7273.","apa":"Horsthemke, M., Bachg, A., Groll, K., Moyzio, S., Müther, B., Hemkemeyer, S., … Hanley, P. (2017). Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. <i>Journal of Biological Chemistry</i>. American Society for Biochemistry and Molecular Biology. <a href=\"https://doi.org/10.1074/jbc.M116.766923\">https://doi.org/10.1074/jbc.M116.766923</a>","ieee":"M. Horsthemke <i>et al.</i>, “Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion,” <i>Journal of Biological Chemistry</i>, vol. 292, no. 17. American Society for Biochemistry and Molecular Biology, pp. 7258–7273, 2017.","ista":"Horsthemke M, Bachg A, Groll K, Moyzio S, Müther B, Hemkemeyer S, Wedlich Söldner R, Sixt MK, Tacke S, Bähler M, Hanley P. 2017. Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. 292(17), 7258–7273.","ama":"Horsthemke M, Bachg A, Groll K, et al. Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. <i>Journal of Biological Chemistry</i>. 2017;292(17):7258-7273. doi:<a href=\"https://doi.org/10.1074/jbc.M116.766923\">10.1074/jbc.M116.766923</a>"},"article_type":"original","publisher":"American Society for Biochemistry and Molecular Biology","_id":"668","article_processing_charge":"No","author":[{"last_name":"Horsthemke","full_name":"Horsthemke, Markus","first_name":"Markus"},{"first_name":"Anne","last_name":"Bachg","full_name":"Bachg, Anne"},{"first_name":"Katharina","last_name":"Groll","full_name":"Groll, Katharina"},{"full_name":"Moyzio, Sven","last_name":"Moyzio","first_name":"Sven"},{"last_name":"Müther","full_name":"Müther, Barbara","first_name":"Barbara"},{"first_name":"Sandra","last_name":"Hemkemeyer","full_name":"Hemkemeyer, Sandra"},{"last_name":"Wedlich Söldner","full_name":"Wedlich Söldner, Roland","first_name":"Roland"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt"},{"first_name":"Sebastian","full_name":"Tacke, Sebastian","last_name":"Tacke"},{"full_name":"Bähler, Martin","last_name":"Bähler","first_name":"Martin"},{"first_name":"Peter","last_name":"Hanley","full_name":"Hanley, Peter"}],"department":[{"_id":"MiSi"}],"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","date_published":"2017-04-28T00:00:00Z","day":"28","year":"2017","publist_id":"7059","status":"public","file":[{"file_id":"6971","relation":"main_file","file_name":"2017_JBC_Horsthemke.pdf","content_type":"application/pdf","checksum":"d488162874326a4bb056065fa549dc4a","creator":"dernst","file_size":5647880,"date_created":"2019-10-24T15:25:42Z","access_level":"open_access","date_updated":"2020-07-14T12:47:37Z"}],"volume":292,"file_date_updated":"2020-07-14T12:47:37Z"},{"publication_identifier":{"issn":["2211-1247"]},"has_accepted_license":"1","issue":"5","tmp":{"short":"CC BY-NC-ND (4.0)","image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"citation":{"mla":"Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” <i>Cell Reports</i>, vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:<a href=\"https://doi.org/10.1016/j.celrep.2017.04.027\">10.1016/j.celrep.2017.04.027</a>.","ista":"Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909.","ama":"Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. <i>Cell Reports</i>. 2017;19(5):902-909. doi:<a href=\"https://doi.org/10.1016/j.celrep.2017.04.027\">10.1016/j.celrep.2017.04.027</a>","short":"K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling, W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909.","chicago":"Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” <i>Cell Reports</i>. Cell Press, 2017. <a href=\"https://doi.org/10.1016/j.celrep.2017.04.027\">https://doi.org/10.1016/j.celrep.2017.04.027</a>.","apa":"Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling, M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. <i>Cell Reports</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.celrep.2017.04.027\">https://doi.org/10.1016/j.celrep.2017.04.027</a>","ieee":"K. Vaahtomeri <i>et al.</i>, “Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia,” <i>Cell Reports</i>, vol. 19, no. 5. Cell Press, pp. 902–909, 2017."},"type":"journal_article","project":[{"grant_number":"281556","call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes"},{"_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes","call_identifier":"FWF","grant_number":"Y 564-B12"}],"quality_controlled":"1","year":"2017","day":"02","date_published":"2017-05-02T00:00:00Z","pubrep_id":"900","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","department":[{"_id":"MiSi"},{"_id":"Bio"},{"_id":"EM-Fac"}],"article_processing_charge":"Yes","_id":"672","author":[{"last_name":"Vaahtomeri","full_name":"Vaahtomeri, Kari","orcid":"0000-0001-7829-3518","first_name":"Kari","id":"368EE576-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Brown","full_name":"Brown, Markus","first_name":"Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Hauschild","full_name":"Hauschild, Robert","orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","first_name":"Robert"},{"full_name":"De Vries, Ingrid","last_name":"De Vries","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid"},{"last_name":"Leithner","full_name":"Leithner, Alexander F","orcid":"0000-0002-1073-744X","first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Mehling","full_name":"Mehling, Matthias","orcid":"0000-0001-8599-1226","id":"3C23B994-F248-11E8-B48F-1D18A9856A87","first_name":"Matthias"},{"last_name":"Kaufmann","full_name":"Kaufmann, Walter","orcid":"0000-0001-9735-5315","id":"3F99E422-F248-11E8-B48F-1D18A9856A87","first_name":"Walter"},{"orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","last_name":"Sixt","full_name":"Sixt, Michael K"}],"publisher":"Cell Press","file_date_updated":"2020-07-14T12:47:38Z","volume":19,"license":"https://creativecommons.org/licenses/by-nc-nd/4.0/","file":[{"creator":"system","checksum":"8fdddaab1f1d76a6ec9ca94dcb6b07a2","file_name":"IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf","content_type":"application/pdf","relation":"main_file","file_id":"5109","date_updated":"2020-07-14T12:47:38Z","access_level":"open_access","file_size":2248814,"date_created":"2018-12-12T10:14:54Z"}],"ec_funded":1,"status":"public","publist_id":"7052","page":"902 - 909","publication":"Cell Reports","date_created":"2018-12-11T11:47:50Z","corr_author":"1","ddc":["570"],"isi":1,"month":"05","intvolume":"        19","oa":1,"oa_version":"Published Version","language":[{"iso":"eng"}],"publication_status":"published","date_updated":"2025-09-10T14:27:34Z","scopus_import":"1","external_id":{"isi":["000402124100002"]},"title":"Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia","abstract":[{"text":"Trafficking cells frequently transmigrate through epithelial and endothelial monolayers. How monolayers cooperate with the penetrating cells to support their transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic capillaries as a model system for transendothelial migration. We find that the chemokine CCL21, which is the decisive guidance cue for intravasation, mainly localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes extracellularly enriched at the sites of endothelial cell-cell junctions. When we reconstitute the transmigration process in vitro, we find that secretion of CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and selective calcium chelation in lymphatic endothelium attenuates transmigration. Altogether, our data demonstrate a chemokine-mediated feedback between DCs and lymphatic endothelium, which facilitates transendothelial migration.","lang":"eng"}],"doi":"10.1016/j.celrep.2017.04.027"},{"citation":{"mla":"Schwarz, Jan, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” <i>Current Biology</i>, vol. 27, no. 9, Cell Press, 2017, pp. 1314–25, doi:<a href=\"https://doi.org/10.1016/j.cub.2017.04.004\">10.1016/j.cub.2017.04.004</a>.","apa":"Schwarz, J., Bierbaum, V., Vaahtomeri, K., Hauschild, R., Brown, M., de Vries, I., … Sixt, M. K. (2017). Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. <i>Current Biology</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.cub.2017.04.004\">https://doi.org/10.1016/j.cub.2017.04.004</a>","ieee":"J. Schwarz <i>et al.</i>, “Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6,” <i>Current Biology</i>, vol. 27, no. 9. Cell Press, pp. 1314–1325, 2017.","chicago":"Schwarz, Jan, Veronika Bierbaum, Kari Vaahtomeri, Robert Hauschild, Markus Brown, Ingrid de Vries, Alexander F Leithner, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” <i>Current Biology</i>. Cell Press, 2017. <a href=\"https://doi.org/10.1016/j.cub.2017.04.004\">https://doi.org/10.1016/j.cub.2017.04.004</a>.","short":"J. Schwarz, V. Bierbaum, K. Vaahtomeri, R. Hauschild, M. Brown, I. de Vries, A.F. Leithner, A. Reversat, J. Merrin, T. Tarrant, M.T. Bollenbach, M.K. Sixt, Current Biology 27 (2017) 1314–1325.","ama":"Schwarz J, Bierbaum V, Vaahtomeri K, et al. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. <i>Current Biology</i>. 2017;27(9):1314-1325. doi:<a href=\"https://doi.org/10.1016/j.cub.2017.04.004\">10.1016/j.cub.2017.04.004</a>","ista":"Schwarz J, Bierbaum V, Vaahtomeri K, Hauschild R, Brown M, de Vries I, Leithner AF, Reversat A, Merrin J, Tarrant T, Bollenbach MT, Sixt MK. 2017. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. 27(9), 1314–1325."},"type":"journal_article","project":[{"call_identifier":"FP7","_id":"25681D80-B435-11E9-9278-68D0E5697425","name":"International IST Postdoc Fellowship Programme","grant_number":"291734"},{"grant_number":"Y 564-B12","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes","call_identifier":"FWF"}],"quality_controlled":"1","publication_identifier":{"issn":["09609822"]},"issue":"9","status":"public","ec_funded":1,"volume":27,"publist_id":"7050","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","department":[{"_id":"MiSi"},{"_id":"Bio"},{"_id":"NanoFab"}],"day":"09","year":"2017","date_published":"2017-05-09T00:00:00Z","publisher":"Cell Press","author":[{"full_name":"Schwarz, Jan","last_name":"Schwarz","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","first_name":"Jan"},{"last_name":"Bierbaum","full_name":"Bierbaum, Veronika","first_name":"Veronika","id":"3FD04378-F248-11E8-B48F-1D18A9856A87"},{"id":"368EE576-F248-11E8-B48F-1D18A9856A87","first_name":"Kari","orcid":"0000-0001-7829-3518","full_name":"Vaahtomeri, Kari","last_name":"Vaahtomeri"},{"last_name":"Hauschild","full_name":"Hauschild, Robert","orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","first_name":"Robert"},{"full_name":"Brown, Markus","last_name":"Brown","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","first_name":"Markus"},{"last_name":"De Vries","full_name":"De Vries, Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid"},{"orcid":"0000-0002-1073-744X","first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","last_name":"Leithner","full_name":"Leithner, Alexander F"},{"first_name":"Anne","id":"35B76592-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-0666-8928","full_name":"Reversat, Anne","last_name":"Reversat"},{"orcid":"0000-0001-5145-4609","first_name":"Jack","id":"4515C308-F248-11E8-B48F-1D18A9856A87","last_name":"Merrin","full_name":"Merrin, Jack"},{"first_name":"Teresa","last_name":"Tarrant","full_name":"Tarrant, Teresa"},{"last_name":"Bollenbach","full_name":"Bollenbach, Tobias","orcid":"0000-0003-4398-476X","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","first_name":"Tobias"},{"orcid":"0000-0002-6620-9179","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","full_name":"Sixt, Michael K"}],"_id":"674","article_processing_charge":"No","intvolume":"        27","publication":"Current Biology","page":"1314 - 1325","date_created":"2018-12-11T11:47:51Z","isi":1,"month":"05","corr_author":"1","abstract":[{"lang":"eng","text":"Navigation of cells along gradients of guidance cues is a determining step in many developmental and immunological processes. Gradients can either be soluble or immobilized to tissues as demonstrated for the haptotactic migration of dendritic cells (DCs) toward higher concentrations of immobilized chemokine CCL21. To elucidate how gradient characteristics govern cellular response patterns, we here introduce an in vitro system allowing to track migratory responses of DCs to precisely controlled immobilized gradients of CCL21. We find that haptotactic sensing depends on the absolute CCL21 concentration and local steepness of the gradient, consistent with a scenario where DC directionality is governed by the signal-to-noise ratio of CCL21 binding to the receptor CCR7. We find that the conditions for optimal DC guidance are perfectly provided by the CCL21 gradients we measure in vivo. Furthermore, we find that CCR7 signal termination by the G-protein-coupled receptor kinase 6 (GRK6) is crucial for haptotactic but dispensable for chemotactic CCL21 gradient sensing in vitro and confirm those observations in vivo. These findings suggest that stable, tissue-bound CCL21 gradients as sustainable “roads” ensure optimal guidance in vivo."}],"title":"Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6","external_id":{"isi":["000400741700021"]},"doi":"10.1016/j.cub.2017.04.004","oa_version":"None","language":[{"iso":"eng"}],"scopus_import":"1","date_updated":"2025-09-10T14:26:47Z","publication_status":"published"},{"scopus_import":"1","publication_status":"published","date_updated":"2025-09-10T14:23:55Z","oa_version":"Published Version","language":[{"iso":"eng"}],"doi":"10.1016/j.celrep.2017.04.051","abstract":[{"text":"The INO80 complex (INO80-C) is an evolutionarily conserved nucleosome remodeler that acts in transcription, replication, and genome stability. It is required for resistance against genotoxic agents and is involved in the repair of DNA double-strand breaks (DSBs) by homologous recombination (HR). However, the causes of the HR defect in INO80-C mutant cells are controversial. Here, we unite previous findings using a system to study HR with high spatial resolution in budding yeast. We find that INO80-C has at least two distinct functions during HR—DNA end resection and presynaptic filament formation. Importantly, the second function is linked to the histone variant H2A.Z. In the absence of H2A.Z, presynaptic filament formation and HR are restored in INO80-C-deficient mutants, suggesting that presynaptic filament formation is the crucial INO80-C function during HR.","lang":"eng"}],"title":"The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination","external_id":{"isi":["000402125100002"]},"ddc":["570"],"isi":1,"month":"05","page":"1294 - 1303","publication":"Cell Reports","date_created":"2018-12-11T11:47:52Z","oa":1,"intvolume":"        19","publisher":"Cell Press","article_processing_charge":"No","_id":"677","author":[{"first_name":"Claudio","last_name":"Lademann","full_name":"Lademann, Claudio"},{"id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","first_name":"Jörg","orcid":"0000-0003-2856-3369","full_name":"Renkawitz, Jörg","last_name":"Renkawitz"},{"full_name":"Pfander, Boris","last_name":"Pfander","first_name":"Boris"},{"full_name":"Jentsch, Stefan","last_name":"Jentsch","first_name":"Stefan"}],"department":[{"_id":"MiSi"}],"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","day":"16","year":"2017","pubrep_id":"899","date_published":"2017-05-16T00:00:00Z","publist_id":"7046","file":[{"date_updated":"2020-07-14T12:47:40Z","access_level":"open_access","file_size":3005610,"date_created":"2018-12-12T10:15:48Z","creator":"system","checksum":"efc7287d9c6354983cb151880e9ad72a","file_name":"IST-2017-899-v1+1_1-s2.0-S2211124717305454-main.pdf","content_type":"application/pdf","relation":"main_file","file_id":"5171"}],"status":"public","volume":19,"file_date_updated":"2020-07-14T12:47:40Z","issue":"7","publication_identifier":{"issn":["2211-1247"]},"has_accepted_license":"1","type":"journal_article","quality_controlled":"1","citation":{"ieee":"C. Lademann, J. Renkawitz, B. Pfander, and S. Jentsch, “The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination,” <i>Cell Reports</i>, vol. 19, no. 7. Cell Press, pp. 1294–1303, 2017.","apa":"Lademann, C., Renkawitz, J., Pfander, B., &#38; Jentsch, S. (2017). The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. <i>Cell Reports</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.celrep.2017.04.051\">https://doi.org/10.1016/j.celrep.2017.04.051</a>","short":"C. Lademann, J. Renkawitz, B. Pfander, S. Jentsch, Cell Reports 19 (2017) 1294–1303.","chicago":"Lademann, Claudio, Jörg Renkawitz, Boris Pfander, and Stefan Jentsch. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” <i>Cell Reports</i>. Cell Press, 2017. <a href=\"https://doi.org/10.1016/j.celrep.2017.04.051\">https://doi.org/10.1016/j.celrep.2017.04.051</a>.","ama":"Lademann C, Renkawitz J, Pfander B, Jentsch S. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. <i>Cell Reports</i>. 2017;19(7):1294-1303. doi:<a href=\"https://doi.org/10.1016/j.celrep.2017.04.051\">10.1016/j.celrep.2017.04.051</a>","ista":"Lademann C, Renkawitz J, Pfander B, Jentsch S. 2017. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. 19(7), 1294–1303.","mla":"Lademann, Claudio, et al. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” <i>Cell Reports</i>, vol. 19, no. 7, Cell Press, 2017, pp. 1294–303, doi:<a href=\"https://doi.org/10.1016/j.celrep.2017.04.051\">10.1016/j.celrep.2017.04.051</a>."},"tmp":{"short":"CC BY-NC-ND (4.0)","image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"}},{"ddc":["570"],"isi":1,"month":"07","page":"2172 - 2184","publication":"Journal of Cell Science","date_created":"2018-12-11T11:47:58Z","oa":1,"intvolume":"       130","date_updated":"2025-09-10T11:13:35Z","publication_status":"published","scopus_import":"1","oa_version":"Published Version","language":[{"iso":"eng"}],"doi":"10.1242/jcs.200899","external_id":{"pmid":["28515231"],"isi":["000405612200009"]},"title":"A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity","abstract":[{"lang":"eng","text":"A change regarding the extent of adhesion - hereafter referred to as adhesion plasticity - between adhesive and less-adhesive states of mammalian cells is important for their behavior. To investigate adhesion plasticity, we have selected a stable isogenic subpopulation of human MDA-MB-468 breast carcinoma cells growing in suspension. These suspension cells are unable to re-adhere to various matrices or to contract three-dimensional collagen lattices. By using transcriptome analysis, we identified the focal adhesion protein tensin3 (Tns3) as a determinant of adhesion plasticity. Tns3 is strongly reduced at mRNA and protein levels in suspension cells. Furthermore, by transiently challenging breast cancer cells to grow under non-adherent conditions markedly reduces Tns3 protein expression, which is regained upon re-adhesion. Stable knockdown of Tns3 in parental MDA-MB-468 cells results in defective adhesion, spreading and migration. Tns3-knockdown cells display impaired structure and dynamics of focal adhesion complexes as determined by immunostaining. Restoration of Tns3 protein expression in suspension cells partially rescues adhesion and focal contact composition. Our work identifies Tns3 as a crucial focal adhesion component regulated by, and functionally contributing to, the switch between adhesive and non-adhesive states in MDA-MB-468 cancer cells."}],"issue":"13","publication_identifier":{"issn":["0021-9533"]},"has_accepted_license":"1","pmid":1,"type":"journal_article","quality_controlled":"1","article_type":"original","citation":{"mla":"Veß, Astrid, et al. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” <i>Journal of Cell Science</i>, vol. 130, no. 13, Company of Biologists, 2017, pp. 2172–84, doi:<a href=\"https://doi.org/10.1242/jcs.200899\">10.1242/jcs.200899</a>.","apa":"Veß, A., Blache, U., Leitner, L., Kurz, A., Ehrenpfordt, A., Sixt, M. K., &#38; Posern, G. (2017). A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. <i>Journal of Cell Science</i>. Company of Biologists. <a href=\"https://doi.org/10.1242/jcs.200899\">https://doi.org/10.1242/jcs.200899</a>","ieee":"A. Veß <i>et al.</i>, “A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity,” <i>Journal of Cell Science</i>, vol. 130, no. 13. Company of Biologists, pp. 2172–2184, 2017.","short":"A. Veß, U. Blache, L. Leitner, A. Kurz, A. Ehrenpfordt, M.K. Sixt, G. Posern, Journal of Cell Science 130 (2017) 2172–2184.","chicago":"Veß, Astrid, Ulrich Blache, Laura Leitner, Angela Kurz, Anja Ehrenpfordt, Michael K Sixt, and Guido Posern. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” <i>Journal of Cell Science</i>. Company of Biologists, 2017. <a href=\"https://doi.org/10.1242/jcs.200899\">https://doi.org/10.1242/jcs.200899</a>.","ama":"Veß A, Blache U, Leitner L, et al. A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. <i>Journal of Cell Science</i>. 2017;130(13):2172-2184. doi:<a href=\"https://doi.org/10.1242/jcs.200899\">10.1242/jcs.200899</a>","ista":"Veß A, Blache U, Leitner L, Kurz A, Ehrenpfordt A, Sixt MK, Posern G. 2017. A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. 130(13), 2172–2184."},"_id":"694","author":[{"full_name":"Veß, Astrid","last_name":"Veß","first_name":"Astrid"},{"full_name":"Blache, Ulrich","last_name":"Blache","first_name":"Ulrich"},{"last_name":"Leitner","full_name":"Leitner, Laura","first_name":"Laura"},{"last_name":"Kurz","full_name":"Kurz, Angela","first_name":"Angela"},{"first_name":"Anja","full_name":"Ehrenpfordt, Anja","last_name":"Ehrenpfordt"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"},{"first_name":"Guido","last_name":"Posern","full_name":"Posern, Guido"}],"article_processing_charge":"No","publisher":"Company of Biologists","year":"2017","day":"01","date_published":"2017-07-01T00:00:00Z","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","department":[{"_id":"MiSi"}],"publist_id":"7008","volume":130,"file_date_updated":"2020-07-14T12:47:45Z","file":[{"creator":"dernst","file_name":"2017_CellScience_Vess.pdf","content_type":"application/pdf","checksum":"42c81a0a4fc3128883b391c3af3f74bc","relation":"main_file","file_id":"6966","date_updated":"2020-07-14T12:47:45Z","access_level":"open_access","file_size":10847596,"date_created":"2019-10-24T09:43:56Z"}],"status":"public"},{"type":"journal_article","quality_controlled":"1","project":[{"grant_number":"LS13-029","_id":"25AD6156-B435-11E9-9278-68D0E5697425","name":"Modeling of Polarization and Motility of Leukocytes in Three-Dimensional Environments"},{"name":"Cytoskeletal force generation and force transduction of migrating leukocytes","_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","grant_number":"281556"}],"citation":{"mla":"Mueller, Jan, et al. “Load Adaptation of Lamellipodial Actin Networks.” <i>Cell</i>, vol. 171, no. 1, Cell Press, 2017, pp. 188–200, doi:<a href=\"https://doi.org/10.1016/j.cell.2017.07.051\">10.1016/j.cell.2017.07.051</a>.","ista":"Mueller J, Szep G, Nemethova M, de Vries I, Lieber A, Winkler C, Kruse K, Small J, Schmeiser C, Keren K, Hauschild R, Sixt MK. 2017. Load adaptation of lamellipodial actin networks. Cell. 171(1), 188–200.","ama":"Mueller J, Szep G, Nemethova M, et al. Load adaptation of lamellipodial actin networks. <i>Cell</i>. 2017;171(1):188-200. doi:<a href=\"https://doi.org/10.1016/j.cell.2017.07.051\">10.1016/j.cell.2017.07.051</a>","chicago":"Mueller, Jan, Gregory Szep, Maria Nemethova, Ingrid de Vries, Arnon Lieber, Christoph Winkler, Karsten Kruse, et al. “Load Adaptation of Lamellipodial Actin Networks.” <i>Cell</i>. Cell Press, 2017. <a href=\"https://doi.org/10.1016/j.cell.2017.07.051\">https://doi.org/10.1016/j.cell.2017.07.051</a>.","short":"J. Mueller, G. Szep, M. Nemethova, I. de Vries, A. Lieber, C. Winkler, K. Kruse, J. Small, C. Schmeiser, K. Keren, R. Hauschild, M.K. Sixt, Cell 171 (2017) 188–200.","ieee":"J. Mueller <i>et al.</i>, “Load adaptation of lamellipodial actin networks,” <i>Cell</i>, vol. 171, no. 1. Cell Press, pp. 188–200, 2017.","apa":"Mueller, J., Szep, G., Nemethova, M., de Vries, I., Lieber, A., Winkler, C., … Sixt, M. K. (2017). Load adaptation of lamellipodial actin networks. <i>Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.cell.2017.07.051\">https://doi.org/10.1016/j.cell.2017.07.051</a>"},"issue":"1","publication_identifier":{"issn":["0092-8674"]},"publist_id":"6951","ec_funded":1,"status":"public","volume":171,"publisher":"Cell Press","_id":"727","article_processing_charge":"No","author":[{"last_name":"Mueller","full_name":"Mueller, Jan","first_name":"Jan"},{"id":"4BFB7762-F248-11E8-B48F-1D18A9856A87","first_name":"Gregory","full_name":"Szep, Gregory","last_name":"Szep"},{"first_name":"Maria","id":"34E27F1C-F248-11E8-B48F-1D18A9856A87","last_name":"Nemethova","full_name":"Nemethova, Maria"},{"id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid","full_name":"De Vries, Ingrid","last_name":"De Vries"},{"full_name":"Lieber, Arnon","last_name":"Lieber","first_name":"Arnon"},{"full_name":"Winkler, Christoph","last_name":"Winkler","first_name":"Christoph"},{"first_name":"Karsten","full_name":"Kruse, Karsten","last_name":"Kruse"},{"last_name":"Small","full_name":"Small, John","first_name":"John"},{"first_name":"Christian","last_name":"Schmeiser","full_name":"Schmeiser, Christian"},{"last_name":"Keren","full_name":"Keren, Kinneret","first_name":"Kinneret"},{"orcid":"0000-0001-9843-3522","first_name":"Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","last_name":"Hauschild","full_name":"Hauschild, Robert"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","department":[{"_id":"MiSi"},{"_id":"Bio"}],"year":"2017","day":"21","date_published":"2017-09-21T00:00:00Z","intvolume":"       171","isi":1,"month":"09","corr_author":"1","page":"188 - 200","publication":"Cell","date_created":"2018-12-11T11:48:10Z","doi":"10.1016/j.cell.2017.07.051","acknowledged_ssus":[{"_id":"ScienComp"}],"title":"Load adaptation of lamellipodial actin networks","abstract":[{"lang":"eng","text":"Actin filaments polymerizing against membranes power endocytosis, vesicular traffic, and cell motility. In vitro reconstitution studies suggest that the structure and the dynamics of actin networks respond to mechanical forces. We demonstrate that lamellipodial actin of migrating cells responds to mechanical load when membrane tension is modulated. In a steady state, migrating cell filaments assume the canonical dendritic geometry, defined by Arp2/3-generated 70° branch points. Increased tension triggers a dense network with a broadened range of angles, whereas decreased tension causes a shift to a sparse configuration dominated by filaments growing perpendicularly to the plasma membrane. We show that these responses emerge from the geometry of branched actin: when load per filament decreases, elongation speed increases and perpendicular filaments gradually outcompete others because they polymerize the shortest distance to the membrane, where they are protected from capping. This network-intrinsic geometrical adaptation mechanism tunes protrusive force in response to mechanical load."}],"external_id":{"isi":["000411331800020"]},"scopus_import":"1","publication_status":"published","date_updated":"2025-07-10T11:54:27Z","oa_version":"None","language":[{"iso":"eng"}]},{"external_id":{"isi":["000399451100002"]},"title":"The dynamic cytokine niche","abstract":[{"text":"Immune cells communicate using cytokine signals, but the quantitative rules of this communication aren't clear. In this issue of Immunity, Oyler-Yaniv et al. (2017) suggest that the distribution of a cytokine within a lymphatic organ is primarily governed by the local density of cells consuming it.","lang":"eng"}],"doi":"10.1016/j.immuni.2017.04.006","oa_version":"None","language":[{"iso":"eng"}],"publication_status":"published","date_updated":"2026-06-05T22:34:18Z","scopus_import":"1","intvolume":"        46","publication":"Immunity","page":"519 - 520","date_created":"2018-12-11T11:47:47Z","corr_author":"1","isi":1,"month":"04","volume":46,"status":"public","publist_id":"7065","day":"18","year":"2017","date_published":"2017-04-18T00:00:00Z","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","department":[{"_id":"MiSi"}],"article_processing_charge":"No","_id":"664","author":[{"first_name":"Frank P","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-3470-6119","full_name":"Assen, Frank P","last_name":"Assen"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}],"publisher":"Cell Press","citation":{"apa":"Assen, F. P., &#38; Sixt, M. K. (2017). The dynamic cytokine niche. <i>Immunity</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.immuni.2017.04.006\">https://doi.org/10.1016/j.immuni.2017.04.006</a>","ieee":"F. P. Assen and M. K. Sixt, “The dynamic cytokine niche,” <i>Immunity</i>, vol. 46, no. 4. Cell Press, pp. 519–520, 2017.","chicago":"Assen, Frank P, and Michael K Sixt. “The Dynamic Cytokine Niche.” <i>Immunity</i>. Cell Press, 2017. <a href=\"https://doi.org/10.1016/j.immuni.2017.04.006\">https://doi.org/10.1016/j.immuni.2017.04.006</a>.","short":"F.P. Assen, M.K. Sixt, Immunity 46 (2017) 519–520.","ama":"Assen FP, Sixt MK. The dynamic cytokine niche. <i>Immunity</i>. 2017;46(4):519-520. doi:<a href=\"https://doi.org/10.1016/j.immuni.2017.04.006\">10.1016/j.immuni.2017.04.006</a>","ista":"Assen FP, Sixt MK. 2017. The dynamic cytokine niche. Immunity. 46(4), 519–520.","mla":"Assen, Frank P., and Michael K. Sixt. “The Dynamic Cytokine Niche.” <i>Immunity</i>, vol. 46, no. 4, Cell Press, 2017, pp. 519–20, doi:<a href=\"https://doi.org/10.1016/j.immuni.2017.04.006\">10.1016/j.immuni.2017.04.006</a>."},"type":"journal_article","quality_controlled":"1","publication_identifier":{"issn":["1074-7613"]},"related_material":{"record":[{"id":"6947","relation":"dissertation_contains","status":"public"}]},"issue":"4"},{"intvolume":"       127","oa":1,"publication":"The Journal of Clinical Investigation","page":"2051 - 2065","date_created":"2018-12-11T11:47:53Z","isi":1,"month":"06","abstract":[{"text":"Protective responses against pathogens require a rapid mobilization of resting neutrophils and the timely removal of activated ones. Neutrophils are exceptionally short-lived leukocytes, yet it remains unclear whether the lifespan of pathogen-engaged neutrophils is regulated differently from that in the circulating steady-state pool. Here, we have found that under homeostatic conditions, the mRNA-destabilizing protein tristetraprolin (TTP) regulates apoptosis and the numbers of activated infiltrating murine neutrophils but not neutrophil cellularity. Activated TTP-deficient neutrophils exhibited decreased apoptosis and enhanced accumulation at the infection site. In the context of myeloid-specific deletion of Ttp, the potentiation of neutrophil deployment protected mice against lethal soft tissue infection with Streptococcus pyogenes and prevented bacterial dissemination. Neutrophil transcriptome analysis revealed that decreased apoptosis of TTP-deficient neutrophils was specifically associated with elevated expression of myeloid cell leukemia 1 (Mcl1) but not other antiapoptotic B cell leukemia/ lymphoma 2 (Bcl2) family members. Higher Mcl1 expression resulted from stabilization of Mcl1 mRNA in the absence of TTP. The low apoptosis rate of infiltrating TTP-deficient neutrophils was comparable to that of transgenic Mcl1-overexpressing neutrophils. Our study demonstrates that posttranscriptional gene regulation by TTP schedules the termination of the antimicrobial engagement of neutrophils. The balancing role of TTP comes at the cost of an increased risk of bacterial infections.","lang":"eng"}],"title":"The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection","external_id":{"isi":["000402620800008"],"pmid":["28504646"]},"doi":"10.1172/JCI80631","oa_version":"Submitted Version","language":[{"iso":"eng"}],"scopus_import":"1","publication_status":"published","date_updated":"2026-06-05T22:34:43Z","citation":{"apa":"Ebner, F., Sedlyarov, V., Tasciyan, S., Ivin, M., Kratochvill, F., Gratz, N., … Kovarik, P. (2017). The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. <i>The Journal of Clinical Investigation</i>. American Society for Clinical Investigation. <a href=\"https://doi.org/10.1172/JCI80631\">https://doi.org/10.1172/JCI80631</a>","ieee":"F. Ebner <i>et al.</i>, “The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection,” <i>The Journal of Clinical Investigation</i>, vol. 127, no. 6. American Society for Clinical Investigation, pp. 2051–2065, 2017.","chicago":"Ebner, Florian, Vitaly Sedlyarov, Saren Tasciyan, Masa Ivin, Franz Kratochvill, Nina Gratz, Lukas Kenner, Andreas Villunger, Michael K Sixt, and Pavel Kovarik. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged Neutrophils during Bacterial Infection.” <i>The Journal of Clinical Investigation</i>. American Society for Clinical Investigation, 2017. <a href=\"https://doi.org/10.1172/JCI80631\">https://doi.org/10.1172/JCI80631</a>.","short":"F. Ebner, V. Sedlyarov, S. Tasciyan, M. Ivin, F. Kratochvill, N. Gratz, L. Kenner, A. Villunger, M.K. Sixt, P. Kovarik, The Journal of Clinical Investigation 127 (2017) 2051–2065.","ama":"Ebner F, Sedlyarov V, Tasciyan S, et al. The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. <i>The Journal of Clinical Investigation</i>. 2017;127(6):2051-2065. doi:<a href=\"https://doi.org/10.1172/JCI80631\">10.1172/JCI80631</a>","ista":"Ebner F, Sedlyarov V, Tasciyan S, Ivin M, Kratochvill F, Gratz N, Kenner L, Villunger A, Sixt MK, Kovarik P. 2017. The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. 127(6), 2051–2065.","mla":"Ebner, Florian, et al. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged Neutrophils during Bacterial Infection.” <i>The Journal of Clinical Investigation</i>, vol. 127, no. 6, American Society for Clinical Investigation, 2017, pp. 2051–65, doi:<a href=\"https://doi.org/10.1172/JCI80631\">10.1172/JCI80631</a>."},"type":"journal_article","quality_controlled":"1","project":[{"grant_number":"T00817-B21","call_identifier":"FWF","name":"The biochemical basis of PAR polarization","_id":"25985A36-B435-11E9-9278-68D0E5697425"},{"name":"Revealing the mechanisms underlying drug interactions","_id":"25E9AF9E-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"P27201-B22"}],"pmid":1,"publication_identifier":{"issn":["0021-9738"]},"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5451238/"}],"issue":"6","related_material":{"record":[{"id":"12401","status":"public","relation":"dissertation_contains"}]},"status":"public","volume":127,"acknowledgement":"This work was supported by grants from the Austrian Science Fund (FWF) (P27538-B21, I1621-B22, and SFB 43, to PK); by funding from the European Union Seventh Framework Programme Marie Curie Initial Training Networks (FP7-PEOPLE-2012-ITN) for the project INBIONET (INfection BIOlogy Training NETwork under grant agreement PITN-GA-2012-316682; and by a joint research cluster initiative of the University of Vienna and the Medical University of Vienna.","publist_id":"7038","department":[{"_id":"MiSi"}],"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","day":"01","year":"2017","date_published":"2017-06-01T00:00:00Z","publisher":"American Society for Clinical Investigation","_id":"679","author":[{"last_name":"Ebner","full_name":"Ebner, Florian","first_name":"Florian"},{"first_name":"Vitaly","full_name":"Sedlyarov, Vitaly","last_name":"Sedlyarov"},{"last_name":"Tasciyan","full_name":"Tasciyan, Saren","orcid":"0000-0003-1671-393X","first_name":"Saren","id":"4323B49C-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Masa","full_name":"Ivin, Masa","last_name":"Ivin"},{"last_name":"Kratochvill","full_name":"Kratochvill, Franz","first_name":"Franz"},{"first_name":"Nina","last_name":"Gratz","full_name":"Gratz, Nina"},{"full_name":"Kenner, Lukas","last_name":"Kenner","first_name":"Lukas"},{"full_name":"Villunger, Andreas","last_name":"Villunger","first_name":"Andreas"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt"},{"full_name":"Kovarik, Pavel","last_name":"Kovarik","first_name":"Pavel"}],"article_processing_charge":"No"},{"type":"journal_article","quality_controlled":"1","citation":{"mla":"Renkawitz, Jörg, and Michael K. Sixt. “A Radical Break Restraining Neutrophil Migration.” <i>Developmental Cell</i>, vol. 38, no. 5, Cell Press, 2016, pp. 448–50, doi:<a href=\"https://doi.org/10.1016/j.devcel.2016.08.017\">10.1016/j.devcel.2016.08.017</a>.","short":"J. Renkawitz, M.K. Sixt, Developmental Cell 38 (2016) 448–450.","chicago":"Renkawitz, Jörg, and Michael K Sixt. “A Radical Break Restraining Neutrophil Migration.” <i>Developmental Cell</i>. Cell Press, 2016. <a href=\"https://doi.org/10.1016/j.devcel.2016.08.017\">https://doi.org/10.1016/j.devcel.2016.08.017</a>.","ieee":"J. Renkawitz and M. K. Sixt, “A Radical Break Restraining Neutrophil Migration,” <i>Developmental Cell</i>, vol. 38, no. 5. Cell Press, pp. 448–450, 2016.","apa":"Renkawitz, J., &#38; Sixt, M. K. (2016). A Radical Break Restraining Neutrophil Migration. <i>Developmental Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.devcel.2016.08.017\">https://doi.org/10.1016/j.devcel.2016.08.017</a>","ama":"Renkawitz J, Sixt MK. A Radical Break Restraining Neutrophil Migration. <i>Developmental Cell</i>. 2016;38(5):448-450. doi:<a href=\"https://doi.org/10.1016/j.devcel.2016.08.017\">10.1016/j.devcel.2016.08.017</a>","ista":"Renkawitz J, Sixt MK. 2016. A Radical Break Restraining Neutrophil Migration. Developmental Cell. 38(5), 448–450."},"issue":"5","publist_id":"6208","volume":38,"status":"public","_id":"1150","article_processing_charge":"No","author":[{"id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","first_name":"Jörg","orcid":"0000-0003-2856-3369","full_name":"Renkawitz, Jörg","last_name":"Renkawitz"},{"full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"}],"publisher":"Cell Press","day":"12","year":"2016","date_published":"2016-09-12T00:00:00Z","department":[{"_id":"MiSi"}],"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","intvolume":"        38","isi":1,"month":"09","publication":"Developmental Cell","page":"448 - 450","date_created":"2018-12-11T11:50:25Z","doi":"10.1016/j.devcel.2016.08.017","external_id":{"isi":["000383413000003"]},"title":"A Radical Break Restraining Neutrophil Migration","abstract":[{"text":"When neutrophils infiltrate a site of inflammation, they have to stop at the right place to exert their effector function. In this issue of Developmental Cell, Wang et al. (2016) show that neutrophils sense reactive oxygen species via the TRPM2 channel to arrest migration at their target site. © 2016 Elsevier Inc.","lang":"eng"}],"publication_status":"published","date_updated":"2025-09-22T09:57:46Z","scopus_import":"1","oa_version":"None","language":[{"iso":"eng"}]},{"has_accepted_license":"1","article_number":"36440","citation":{"chicago":"Schwarz, Jan, Veronika Bierbaum, Jack Merrin, Tino Frank, Robert Hauschild, Mark Tobias Bollenbach, Savaş Tay, Michael K Sixt, and Matthias Mehling. “A Microfluidic Device for Measuring Cell Migration towards Substrate Bound and Soluble Chemokine Gradients.” <i>Scientific Reports</i>. Nature Publishing Group, 2016. <a href=\"https://doi.org/10.1038/srep36440\">https://doi.org/10.1038/srep36440</a>.","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).","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. <i>Scientific Reports</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/srep36440\">https://doi.org/10.1038/srep36440</a>","ieee":"J. Schwarz <i>et al.</i>, “A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients,” <i>Scientific Reports</i>, 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.","ama":"Schwarz J, Bierbaum V, Merrin J, et al. A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients. <i>Scientific Reports</i>. 2016;6. doi:<a href=\"https://doi.org/10.1038/srep36440\">10.1038/srep36440</a>","mla":"Schwarz, Jan, et al. “A Microfluidic Device for Measuring Cell Migration towards Substrate Bound and Soluble Chemokine Gradients.” <i>Scientific Reports</i>, vol. 6, 36440, Nature Publishing Group, 2016, doi:<a href=\"https://doi.org/10.1038/srep36440\">10.1038/srep36440</a>."},"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","quality_controlled":"1","project":[{"name":"Cytoskeletal force generation and force transduction of migrating leukocytes","_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","grant_number":"281556"},{"name":"Cytoskeletal force generation and force transduction of migrating leukocytes","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"Y 564-B12"}],"department":[{"_id":"MiSi"},{"_id":"NanoFab"},{"_id":"Bio"},{"_id":"ToBo"}],"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","day":"07","year":"2016","date_published":"2016-11-07T00:00:00Z","pubrep_id":"744","publisher":"Nature Publishing Group","_id":"1154","article_processing_charge":"No","author":[{"first_name":"Jan","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","last_name":"Schwarz","full_name":"Schwarz, Jan"},{"first_name":"Veronika","id":"3FD04378-F248-11E8-B48F-1D18A9856A87","full_name":"Bierbaum, Veronika","last_name":"Bierbaum"},{"full_name":"Merrin, Jack","last_name":"Merrin","first_name":"Jack","id":"4515C308-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5145-4609"},{"full_name":"Frank, Tino","last_name":"Frank","first_name":"Tino"},{"id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","first_name":"Robert","orcid":"0000-0001-9843-3522","full_name":"Hauschild, Robert","last_name":"Hauschild"},{"orcid":"0000-0003-4398-476X","first_name":"Mark Tobias","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","last_name":"Bollenbach","full_name":"Bollenbach, Mark Tobias"},{"first_name":"Savaş","full_name":"Tay, Savaş","last_name":"Tay"},{"orcid":"0000-0002-6620-9179","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","full_name":"Sixt, Michael K"},{"last_name":"Mehling","full_name":"Mehling, Matthias","orcid":"0000-0001-8599-1226","id":"3C23B994-F248-11E8-B48F-1D18A9856A87","first_name":"Matthias"}],"file":[{"access_level":"open_access","date_updated":"2018-12-12T10:09:32Z","date_created":"2018-12-12T10:09:32Z","file_size":2353456,"content_type":"application/pdf","file_name":"IST-2017-744-v1+1_srep36440.pdf","creator":"system","file_id":"4756","relation":"main_file"}],"status":"public","ec_funded":1,"volume":6,"file_date_updated":"2018-12-12T10:09:32Z","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","publist_id":"6204","publication":"Scientific Reports","date_created":"2018-12-11T11:50:27Z","isi":1,"ddc":["579"],"month":"11","intvolume":"         6","oa":1,"oa_version":"Published Version","language":[{"iso":"eng"}],"scopus_import":"1","date_updated":"2025-09-22T09:56:13Z","publication_status":"published","title":"A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients","abstract":[{"text":"Cellular locomotion is a central hallmark of eukaryotic life. It is governed by cell-extrinsic molecular factors, which can either emerge in the soluble phase or as immobilized, often adhesive ligands. To encode for direction, every cue must be present as a spatial or temporal gradient. Here, we developed a microfluidic chamber that allows measurement of cell migration in combined response to surface immobilized and soluble molecular gradients. As a proof of principle we study the response of dendritic cells to their major guidance cues, chemokines. The majority of data on chemokine gradient sensing is based on in vitro studies employing soluble gradients. Despite evidence suggesting that in vivo chemokines are often immobilized to sugar residues, limited information is available how cells respond to immobilized chemokines. We tracked migration of dendritic cells towards immobilized gradients of the chemokine CCL21 and varying superimposed soluble gradients of CCL19. Differential migratory patterns illustrate the potential of our setup to quantitatively study the competitive response to both types of gradients. Beyond chemokines our approach is broadly applicable to alternative systems of chemo- and haptotaxis such as cells migrating along gradients of adhesion receptor ligands vs. any soluble cue. \r\n","lang":"eng"}],"external_id":{"isi":["000387118300001"]},"doi":"10.1038/srep36440"},{"abstract":[{"text":"In this issue of Cell, Skau et al. show that the formin FMN2 organizes a perinuclear actin cytoskeleton that protects the nucleus and its genomic content of migrating cells squeezing through small spaces.","lang":"eng"}],"title":"Formin’ a nuclear protection","external_id":{"isi":["000389470500007"]},"doi":"10.1016/j.cell.2016.11.024","language":[{"iso":"eng"}],"oa_version":"None","scopus_import":"1","date_updated":"2025-09-22T09:41:33Z","publication_status":"published","intvolume":"       167","date_created":"2018-12-11T11:50:41Z","page":"1448 - 1449","publication":"Cell","month":"12","isi":1,"status":"public","volume":167,"publist_id":"6149","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","department":[{"_id":"MiSi"}],"date_published":"2016-12-01T00:00:00Z","day":"01","year":"2016","publisher":"Cell Press","_id":"1201","author":[{"orcid":"0000-0003-2856-3369","first_name":"Jörg","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","last_name":"Renkawitz","full_name":"Renkawitz, Jörg"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}],"article_processing_charge":"No","citation":{"mla":"Renkawitz, Jörg, and Michael K. Sixt. “Formin’ a Nuclear Protection.” <i>Cell</i>, vol. 167, no. 6, Cell Press, 2016, pp. 1448–49, doi:<a href=\"https://doi.org/10.1016/j.cell.2016.11.024\">10.1016/j.cell.2016.11.024</a>.","ista":"Renkawitz J, Sixt MK. 2016. Formin’ a nuclear protection. Cell. 167(6), 1448–1449.","ama":"Renkawitz J, Sixt MK. Formin’ a nuclear protection. <i>Cell</i>. 2016;167(6):1448-1449. doi:<a href=\"https://doi.org/10.1016/j.cell.2016.11.024\">10.1016/j.cell.2016.11.024</a>","apa":"Renkawitz, J., &#38; Sixt, M. K. (2016). Formin’ a nuclear protection. <i>Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.cell.2016.11.024\">https://doi.org/10.1016/j.cell.2016.11.024</a>","ieee":"J. Renkawitz and M. K. Sixt, “Formin’ a nuclear protection,” <i>Cell</i>, vol. 167, no. 6. Cell Press, pp. 1448–1449, 2016.","chicago":"Renkawitz, Jörg, and Michael K Sixt. “Formin’ a Nuclear Protection.” <i>Cell</i>. Cell Press, 2016. <a href=\"https://doi.org/10.1016/j.cell.2016.11.024\">https://doi.org/10.1016/j.cell.2016.11.024</a>.","short":"J. Renkawitz, M.K. Sixt, Cell 167 (2016) 1448–1449."},"quality_controlled":"1","type":"journal_article","issue":"6"}]