[{"date_updated":"2024-03-27T23:30:39Z","department":[{"_id":"MiSi"},{"_id":"Bio"}],"_id":"15","status":"public","type":"journal_article","language":[{"iso":"eng"}],"publication_status":"published","volume":19,"issue":"6","related_material":{"record":[{"id":"6891","status":"public","relation":"dissertation_contains"}]},"ec_funded":1,"pmid":1,"oa_version":"Published Version","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"}],"acknowledged_ssus":[{"_id":"SSU"}],"month":"05","intvolume":" 19","scopus_import":"1","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pubmed/29777221"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"chicago":"Hons, Miroslav, Aglaja Kopf, Robert Hauschild, Alexander F Leithner, Florian R Gärtner, Jun Abe, Jörg Renkawitz, Jens Stein, and Michael K Sixt. “Chemokines and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal Migration of T Cells.” Nature Immunology. Nature Publishing Group, 2018. https://doi.org/10.1038/s41590-018-0109-z.","ista":"Hons M, Kopf A, Hauschild R, Leithner AF, Gärtner FR, Abe J, Renkawitz J, Stein J, Sixt MK. 2018. Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. Nature Immunology. 19(6), 606–616.","mla":"Hons, Miroslav, et al. “Chemokines and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal Migration of T Cells.” Nature Immunology, vol. 19, no. 6, Nature Publishing Group, 2018, pp. 606–16, doi:10.1038/s41590-018-0109-z.","apa":"Hons, M., Kopf, A., Hauschild, R., Leithner, A. F., Gärtner, F. R., Abe, J., … Sixt, M. K. (2018). Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/s41590-018-0109-z","ama":"Hons M, Kopf A, Hauschild R, et al. Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. Nature Immunology. 2018;19(6):606-616. doi:10.1038/s41590-018-0109-z","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.","ieee":"M. Hons et al., “Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells,” Nature Immunology, vol. 19, no. 6. Nature Publishing Group, pp. 606–616, 2018."},"title":"Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells","author":[{"id":"4167FE56-F248-11E8-B48F-1D18A9856A87","first_name":"Miroslav","full_name":"Hons, Miroslav","orcid":"0000-0002-6625-3348","last_name":"Hons"},{"last_name":"Kopf","orcid":"0000-0002-2187-6656","full_name":"Kopf, Aglaja","first_name":"Aglaja","id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Hauschild","full_name":"Hauschild, Robert","orcid":"0000-0001-9843-3522","first_name":"Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87"},{"id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander F","last_name":"Leithner","orcid":"0000-0002-1073-744X","full_name":"Leithner, Alexander F"},{"first_name":"Florian R","id":"397A88EE-F248-11E8-B48F-1D18A9856A87","last_name":"Gärtner","orcid":"0000-0001-6120-3723","full_name":"Gärtner, Florian R"},{"first_name":"Jun","full_name":"Abe, Jun","last_name":"Abe"},{"full_name":"Renkawitz, Jörg","orcid":"0000-0003-2856-3369","last_name":"Renkawitz","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","first_name":"Jörg"},{"full_name":"Stein, Jens","last_name":"Stein","first_name":"Jens"},{"last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}],"publist_id":"8040","article_processing_charge":"No","external_id":{"pmid":["29777221"],"isi":["000433041500026"]},"project":[{"call_identifier":"H2020","_id":"25FE9508-B435-11E9-9278-68D0E5697425","name":"Cellular navigation along spatial gradients","grant_number":"724373"},{"name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells","grant_number":"747687","_id":"260AA4E2-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"_id":"25A48D24-B435-11E9-9278-68D0E5697425","grant_number":"ALTF 1396-2014","name":"Molecular and system level view of immune cell migration"},{"call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","grant_number":"281556","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)"}],"day":"18","publication":"Nature Immunology","isi":1,"year":"2018","doi":"10.1038/s41590-018-0109-z","date_published":"2018-05-18T00:00:00Z","date_created":"2018-12-11T11:44:10Z","page":"606 - 616","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).","publisher":"Nature Publishing Group","quality_controlled":"1","oa":1},{"title":"Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments","publist_id":"7245","author":[{"first_name":"Felix","last_name":"Spira","full_name":"Spira, Felix"},{"first_name":"Sara","last_name":"Cuylen Haering","full_name":"Cuylen Haering, Sara"},{"first_name":"Shalin","full_name":"Mehta, Shalin","last_name":"Mehta"},{"last_name":"Samwer","full_name":"Samwer, Matthias","first_name":"Matthias"},{"id":"35B76592-F248-11E8-B48F-1D18A9856A87","first_name":"Anne","last_name":"Reversat","orcid":"0000-0003-0666-8928","full_name":"Reversat, Anne"},{"full_name":"Verma, Amitabh","last_name":"Verma","first_name":"Amitabh"},{"first_name":"Rudolf","last_name":"Oldenbourg","full_name":"Oldenbourg, Rudolf"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"},{"full_name":"Gerlich, Daniel","last_name":"Gerlich","first_name":"Daniel"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"Spira, Felix, et al. “Cytokinesis in Vertebrate Cells Initiates by Contraction of an Equatorial Actomyosin Network Composed of Randomly Oriented Filaments.” ELife, vol. 6, e30867, eLife Sciences Publications, 2017, doi:10.7554/eLife.30867.","ieee":"F. Spira et al., “Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments,” eLife, vol. 6. eLife Sciences Publications, 2017.","short":"F. Spira, S. Cuylen Haering, S. Mehta, M. Samwer, A. Reversat, A. Verma, R. Oldenbourg, M.K. Sixt, D. Gerlich, ELife 6 (2017).","ama":"Spira F, Cuylen Haering S, Mehta S, et al. Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. eLife. 2017;6. doi:10.7554/eLife.30867","apa":"Spira, F., Cuylen Haering, S., Mehta, S., Samwer, M., Reversat, A., Verma, A., … Gerlich, D. (2017). Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.30867","chicago":"Spira, Felix, Sara Cuylen Haering, Shalin Mehta, Matthias Samwer, Anne Reversat, Amitabh Verma, Rudolf Oldenbourg, Michael K Sixt, and Daniel Gerlich. “Cytokinesis in Vertebrate Cells Initiates by Contraction of an Equatorial Actomyosin Network Composed of Randomly Oriented Filaments.” ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.30867.","ista":"Spira F, Cuylen Haering S, Mehta S, Samwer M, Reversat A, Verma A, Oldenbourg R, Sixt MK, Gerlich D. 2017. Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. eLife. 6, e30867."},"article_number":"e30867","doi":"10.7554/eLife.30867","date_published":"2017-11-06T00:00:00Z","date_created":"2018-12-11T11:47:14Z","day":"06","publication":"eLife","has_accepted_license":"1","year":"2017","publisher":"eLife Sciences Publications","quality_controlled":"1","oa":1,"file_date_updated":"2020-07-14T12:47:10Z","department":[{"_id":"MiSi"}],"ddc":["570"],"date_updated":"2023-02-23T12:30:29Z","status":"public","pubrep_id":"919","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"_id":"569","volume":6,"file":[{"relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_id":"4829","checksum":"ba09c1451153d39e4f4b7cee013e314c","creator":"system","file_size":9666973,"date_updated":"2020-07-14T12:47:10Z","file_name":"IST-2017-919-v1+1_elife-30867-figures-v1.pdf","date_created":"2018-12-12T10:10:40Z"},{"file_size":5951246,"date_updated":"2020-07-14T12:47:10Z","creator":"system","file_name":"IST-2017-919-v1+2_elife-30867-v1.pdf","date_created":"2018-12-12T10:10:41Z","content_type":"application/pdf","relation":"main_file","access_level":"open_access","checksum":"01eb51f1d6ad679947415a51c988e137","file_id":"4830"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2050084X"]},"publication_status":"published","month":"11","intvolume":" 6","scopus_import":1,"oa_version":"Published Version","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"}]},{"abstract":[{"text":"Blood platelets are critical for hemostasis and thrombosis and play diverse roles during immune responses. Despite these versatile tasks in mammalian biology, their skills on a cellular level are deemed limited, mainly consisting in rolling, adhesion, and aggregate formation. Here, we identify an unappreciated asset of platelets and show that adherent platelets use adhesion receptors to mechanically probe the adhesive substrate in their local microenvironment. When actomyosin-dependent traction forces overcome substrate resistance, platelets migrate and pile up the adhesive substrate together with any bound particulate material. They use this ability to act as cellular scavengers, scanning the vascular surface for potential invaders and collecting deposited bacteria. Microbe collection by migrating platelets boosts the activity of professional phagocytes, exacerbating inflammatory tissue injury in sepsis. This assigns platelets a central role in innate immune responses and identifies them as potential targets to dampen inflammatory tissue damage in clinical scenarios of severe systemic infection. In addition to their role in thrombosis and hemostasis, platelets can also migrate to sites of infection to help trap bacteria and clear the vascular surface.","lang":"eng"}],"oa_version":"None","scopus_import":1,"month":"11","intvolume":" 171","publication_identifier":{"issn":["00928674"]},"publication_status":"published","language":[{"iso":"eng"}],"volume":171,"issue":"6","ec_funded":1,"_id":"571","type":"journal_article","status":"public","date_updated":"2021-01-12T08:03:15Z","department":[{"_id":"MiSi"}],"publisher":"Cell Press","quality_controlled":"1","year":"2017","day":"30","publication":"Cell Press","page":"1368 - 1382","date_published":"2017-11-30T00:00:00Z","doi":"10.1016/j.cell.2017.11.001","date_created":"2018-12-11T11:47:15Z","project":[{"call_identifier":"H2020","_id":"260AA4E2-B435-11E9-9278-68D0E5697425","grant_number":"747687","name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells"}],"citation":{"mla":"Gärtner, Florian R., et al. “Migrating Platelets Are Mechano Scavengers That Collect and Bundle Bacteria.” Cell Press, vol. 171, no. 6, Cell Press, 2017, pp. 1368–82, doi:10.1016/j.cell.2017.11.001.","ama":"Gärtner FR, Ahmad Z, Rosenberger G, et al. Migrating platelets are mechano scavengers that collect and bundle bacteria. Cell Press. 2017;171(6):1368-1382. doi:10.1016/j.cell.2017.11.001","apa":"Gärtner, F. R., Ahmad, Z., Rosenberger, G., Fan, S., Nicolai, L., Busch, B., … Massberg, S. (2017). Migrating platelets are mechano scavengers that collect and bundle bacteria. Cell Press. Cell Press. https://doi.org/10.1016/j.cell.2017.11.001","short":"F.R. Gärtner, Z. Ahmad, G. Rosenberger, S. Fan, L. Nicolai, B. Busch, G. Yavuz, M. Luckner, H. Ishikawa Ankerhold, R. Hennel, A. Benechet, M. Lorenz, S. Chandraratne, I. Schubert, S. Helmer, B. Striednig, K. Stark, M. Janko, R. Böttcher, A. Verschoor, C. Leon, C. Gachet, T. Gudermann, M. Mederos Y Schnitzler, Z. Pincus, M. Iannacone, R. Haas, G. Wanner, K. Lauber, M.K. Sixt, S. Massberg, Cell Press 171 (2017) 1368–1382.","ieee":"F. R. Gärtner et al., “Migrating platelets are mechano scavengers that collect and bundle bacteria,” Cell Press, vol. 171, no. 6. Cell Press, pp. 1368–1382, 2017.","chicago":"Gärtner, Florian R, Zerkah Ahmad, Gerhild Rosenberger, Shuxia Fan, Leo Nicolai, Benjamin Busch, Gökce Yavuz, et al. “Migrating Platelets Are Mechano Scavengers That Collect and Bundle Bacteria.” Cell Press. Cell Press, 2017. https://doi.org/10.1016/j.cell.2017.11.001.","ista":"Gärtner FR, Ahmad Z, Rosenberger G, Fan S, Nicolai L, Busch B, Yavuz G, Luckner M, Ishikawa Ankerhold H, Hennel R, Benechet A, Lorenz M, Chandraratne S, Schubert I, Helmer S, Striednig B, Stark K, Janko M, Böttcher R, Verschoor A, Leon C, Gachet C, Gudermann T, Mederos Y Schnitzler M, Pincus Z, Iannacone M, Haas R, Wanner G, Lauber K, Sixt MK, Massberg S. 2017. Migrating platelets are mechano scavengers that collect and bundle bacteria. Cell Press. 171(6), 1368–1382."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publist_id":"7243","author":[{"last_name":"Gärtner","full_name":"Gärtner, Florian R","orcid":"0000-0001-6120-3723","id":"397A88EE-F248-11E8-B48F-1D18A9856A87","first_name":"Florian R"},{"first_name":"Zerkah","last_name":"Ahmad","full_name":"Ahmad, Zerkah"},{"first_name":"Gerhild","last_name":"Rosenberger","full_name":"Rosenberger, Gerhild"},{"first_name":"Shuxia","last_name":"Fan","full_name":"Fan, Shuxia"},{"first_name":"Leo","full_name":"Nicolai, Leo","last_name":"Nicolai"},{"first_name":"Benjamin","full_name":"Busch, Benjamin","last_name":"Busch"},{"full_name":"Yavuz, Gökce","last_name":"Yavuz","first_name":"Gökce"},{"full_name":"Luckner, Manja","last_name":"Luckner","first_name":"Manja"},{"first_name":"Hellen","last_name":"Ishikawa Ankerhold","full_name":"Ishikawa Ankerhold, Hellen"},{"first_name":"Roman","full_name":"Hennel, Roman","last_name":"Hennel"},{"first_name":"Alexandre","last_name":"Benechet","full_name":"Benechet, Alexandre"},{"first_name":"Michael","full_name":"Lorenz, Michael","last_name":"Lorenz"},{"full_name":"Chandraratne, Sue","last_name":"Chandraratne","first_name":"Sue"},{"full_name":"Schubert, Irene","last_name":"Schubert","first_name":"Irene"},{"first_name":"Sebastian","full_name":"Helmer, Sebastian","last_name":"Helmer"},{"full_name":"Striednig, Bianca","last_name":"Striednig","first_name":"Bianca"},{"last_name":"Stark","full_name":"Stark, Konstantin","first_name":"Konstantin"},{"first_name":"Marek","last_name":"Janko","full_name":"Janko, Marek"},{"last_name":"Böttcher","full_name":"Böttcher, Ralph","first_name":"Ralph"},{"first_name":"Admar","last_name":"Verschoor","full_name":"Verschoor, Admar"},{"full_name":"Leon, Catherine","last_name":"Leon","first_name":"Catherine"},{"full_name":"Gachet, Christian","last_name":"Gachet","first_name":"Christian"},{"first_name":"Thomas","full_name":"Gudermann, Thomas","last_name":"Gudermann"},{"first_name":"Michael","full_name":"Mederos Y Schnitzler, Michael","last_name":"Mederos Y Schnitzler"},{"last_name":"Pincus","full_name":"Pincus, Zachary","first_name":"Zachary"},{"first_name":"Matteo","last_name":"Iannacone","full_name":"Iannacone, Matteo"},{"first_name":"Rainer","last_name":"Haas","full_name":"Haas, Rainer"},{"first_name":"Gerhard","full_name":"Wanner, Gerhard","last_name":"Wanner"},{"first_name":"Kirsten","full_name":"Lauber, Kirsten","last_name":"Lauber"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Massberg, Steffen","last_name":"Massberg","first_name":"Steffen"}],"title":"Migrating platelets are mechano scavengers that collect and bundle bacteria"},{"file_date_updated":"2020-07-14T12:47:34Z","department":[{"_id":"MiSi"}],"date_updated":"2021-01-12T08:08:06Z","ddc":["570"],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","pubrep_id":"902","status":"public","_id":"659","volume":8,"publication_status":"published","publication_identifier":{"issn":["20411723"]},"language":[{"iso":"eng"}],"file":[{"relation":"main_file","access_level":"open_access","content_type":"application/pdf","checksum":"dae30190291c3630e8102d8714a8d23e","file_id":"5072","creator":"system","file_size":9523746,"date_updated":"2020-07-14T12:47:34Z","file_name":"IST-2017-902-v1+1_Kage_et_al-2017-Nature_Communications.pdf","date_created":"2018-12-12T10:14:21Z"}],"scopus_import":1,"intvolume":" 8","month":"03","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"}],"oa_version":"Published Version","article_processing_charge":"No","publist_id":"7075","author":[{"full_name":"Kage, Frieda","last_name":"Kage","first_name":"Frieda"},{"full_name":"Winterhoff, Moritz","last_name":"Winterhoff","first_name":"Moritz"},{"last_name":"Dimchev","full_name":"Dimchev, Vanessa","first_name":"Vanessa"},{"first_name":"Jan","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D","full_name":"Müller, Jan","last_name":"Müller"},{"last_name":"Thalheim","full_name":"Thalheim, Tobias","first_name":"Tobias"},{"first_name":"Anika","full_name":"Freise, Anika","last_name":"Freise"},{"last_name":"Brühmann","full_name":"Brühmann, Stefan","first_name":"Stefan"},{"last_name":"Kollasser","full_name":"Kollasser, Jana","first_name":"Jana"},{"first_name":"Jennifer","full_name":"Block, Jennifer","last_name":"Block"},{"full_name":"Dimchev, Georgi A","last_name":"Dimchev","first_name":"Georgi A"},{"first_name":"Matthias","last_name":"Geyer","full_name":"Geyer, Matthias"},{"full_name":"Schnittler, Hams","last_name":"Schnittler","first_name":"Hams"},{"last_name":"Brakebusch","full_name":"Brakebusch, Cord","first_name":"Cord"},{"first_name":"Theresia","last_name":"Stradal","full_name":"Stradal, Theresia"},{"full_name":"Carlier, Marie","last_name":"Carlier","first_name":"Marie"},{"last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"},{"last_name":"Käs","full_name":"Käs, Josef","first_name":"Josef"},{"first_name":"Jan","full_name":"Faix, Jan","last_name":"Faix"},{"full_name":"Rottner, Klemens","last_name":"Rottner","first_name":"Klemens"}],"title":"FMNL formins boost lamellipodial force generation","citation":{"chicago":"Kage, Frieda, Moritz Winterhoff, Vanessa Dimchev, Jan Müller, Tobias Thalheim, Anika Freise, Stefan Brühmann, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/ncomms14832.","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.","mla":"Kage, Frieda, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature Communications, vol. 8, 14832, Nature Publishing Group, 2017, doi:10.1038/ncomms14832.","apa":"Kage, F., Winterhoff, M., Dimchev, V., Müller, J., Thalheim, T., Freise, A., … Rottner, K. (2017). FMNL formins boost lamellipodial force generation. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms14832","ama":"Kage F, Winterhoff M, Dimchev V, et al. FMNL formins boost lamellipodial force generation. Nature Communications. 2017;8. doi:10.1038/ncomms14832","ieee":"F. Kage et al., “FMNL formins boost lamellipodial force generation,” Nature Communications, vol. 8. Nature Publishing Group, 2017.","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)."},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","article_number":"14832","date_created":"2018-12-11T11:47:46Z","date_published":"2017-03-22T00:00:00Z","doi":"10.1038/ncomms14832","year":"2017","has_accepted_license":"1","publication":"Nature Communications","day":"22","oa":1,"quality_controlled":"1","publisher":"Nature Publishing Group"},{"citation":{"ama":"Horsthemke M, Bachg A, Groll K, et al. Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. 2017;292(17):7258-7273. doi:10.1074/jbc.M116.766923","apa":"Horsthemke, M., Bachg, A., Groll, K., Moyzio, S., Müther, B., Hemkemeyer, S., … Hanley, P. (2017). Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. American Society for Biochemistry and Molecular Biology. https://doi.org/10.1074/jbc.M116.766923","ieee":"M. Horsthemke et al., “Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion,” Journal of Biological Chemistry, vol. 292, no. 17. American Society for Biochemistry and Molecular Biology, pp. 7258–7273, 2017.","short":"M. Horsthemke, A. Bachg, K. Groll, S. Moyzio, B. Müther, S. Hemkemeyer, R. Wedlich Söldner, M.K. Sixt, S. Tacke, M. Bähler, P. Hanley, Journal of Biological Chemistry 292 (2017) 7258–7273.","mla":"Horsthemke, Markus, et al. “Multiple Roles of Filopodial Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal of Biological Chemistry, vol. 292, no. 17, American Society for Biochemistry and Molecular Biology, 2017, pp. 7258–73, doi:10.1074/jbc.M116.766923.","ista":"Horsthemke M, Bachg A, Groll K, Moyzio S, Müther B, Hemkemeyer S, Wedlich Söldner R, Sixt MK, Tacke S, Bähler M, Hanley P. 2017. Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. 292(17), 7258–7273.","chicago":"Horsthemke, Markus, Anne Bachg, Katharina Groll, Sven Moyzio, Barbara Müther, Sandra Hemkemeyer, Roland Wedlich Söldner, et al. “Multiple Roles of Filopodial Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal of Biological Chemistry. American Society for Biochemistry and Molecular Biology, 2017. https://doi.org/10.1074/jbc.M116.766923."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"first_name":"Markus","full_name":"Horsthemke, Markus","last_name":"Horsthemke"},{"full_name":"Bachg, Anne","last_name":"Bachg","first_name":"Anne"},{"last_name":"Groll","full_name":"Groll, Katharina","first_name":"Katharina"},{"first_name":"Sven","full_name":"Moyzio, Sven","last_name":"Moyzio"},{"last_name":"Müther","full_name":"Müther, Barbara","first_name":"Barbara"},{"first_name":"Sandra","full_name":"Hemkemeyer, Sandra","last_name":"Hemkemeyer"},{"full_name":"Wedlich Söldner, Roland","last_name":"Wedlich Söldner","first_name":"Roland"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"},{"full_name":"Tacke, Sebastian","last_name":"Tacke","first_name":"Sebastian"},{"last_name":"Bähler","full_name":"Bähler, Martin","first_name":"Martin"},{"first_name":"Peter","last_name":"Hanley","full_name":"Hanley, Peter"}],"publist_id":"7059","title":"Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion","year":"2017","has_accepted_license":"1","publication":"Journal of Biological Chemistry","day":"28","page":"7258 - 7273","date_created":"2018-12-11T11:47:49Z","date_published":"2017-04-28T00:00:00Z","doi":"10.1074/jbc.M116.766923","oa":1,"publisher":"American Society for Biochemistry and Molecular Biology","quality_controlled":"1","date_updated":"2021-01-12T08:08:34Z","ddc":["570"],"department":[{"_id":"MiSi"}],"file_date_updated":"2020-07-14T12:47:37Z","_id":"668","type":"journal_article","article_type":"original","status":"public","publication_status":"published","publication_identifier":{"issn":["00219258"]},"language":[{"iso":"eng"}],"file":[{"file_id":"6971","checksum":"d488162874326a4bb056065fa549dc4a","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"2017_JBC_Horsthemke.pdf","date_created":"2019-10-24T15:25:42Z","creator":"dernst","file_size":5647880,"date_updated":"2020-07-14T12:47:37Z"}],"issue":"17","volume":292,"abstract":[{"lang":"eng","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."}],"oa_version":"Published Version","scopus_import":1,"intvolume":" 292","month":"04"},{"project":[{"name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556","call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425"},{"grant_number":"Y 564-B12","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","call_identifier":"FWF","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425"}],"title":"Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia","article_processing_charge":"Yes","author":[{"orcid":"0000-0001-7829-3518","full_name":"Vaahtomeri, Kari","last_name":"Vaahtomeri","first_name":"Kari","id":"368EE576-F248-11E8-B48F-1D18A9856A87"},{"id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","first_name":"Markus","full_name":"Brown, Markus","last_name":"Brown"},{"full_name":"Hauschild, Robert","orcid":"0000-0001-9843-3522","last_name":"Hauschild","first_name":"Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87"},{"last_name":"De Vries","full_name":"De Vries, Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid"},{"first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","last_name":"Leithner","full_name":"Leithner, Alexander F"},{"first_name":"Matthias","id":"3C23B994-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8599-1226","full_name":"Mehling, Matthias","last_name":"Mehling"},{"id":"3F99E422-F248-11E8-B48F-1D18A9856A87","first_name":"Walter","orcid":"0000-0001-9735-5315","full_name":"Kaufmann, Walter","last_name":"Kaufmann"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}],"publist_id":"7052","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.027.","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.","mla":"Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports, vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:10.1016/j.celrep.2017.04.027.","ieee":"K. Vaahtomeri et al., “Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia,” Cell Reports, vol. 19, no. 5. Cell Press, pp. 902–909, 2017.","short":"K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling, W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909.","apa":"Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling, M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.027","ama":"Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 2017;19(5):902-909. doi:10.1016/j.celrep.2017.04.027"},"oa":1,"quality_controlled":"1","publisher":"Cell Press","date_created":"2018-12-11T11:47:50Z","doi":"10.1016/j.celrep.2017.04.027","date_published":"2017-05-02T00:00:00Z","page":"902 - 909","publication":"Cell Reports","day":"02","year":"2017","has_accepted_license":"1","pubrep_id":"900","status":"public","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"type":"journal_article","_id":"672","department":[{"_id":"MiSi"},{"_id":"Bio"},{"_id":"EM-Fac"}],"file_date_updated":"2020-07-14T12:47:38Z","ddc":["570"],"date_updated":"2023-02-23T12:50:09Z","intvolume":" 19","month":"05","scopus_import":1,"oa_version":"Published Version","abstract":[{"lang":"eng","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."}],"ec_funded":1,"issue":"5","volume":19,"language":[{"iso":"eng"}],"file":[{"content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_id":"5109","checksum":"8fdddaab1f1d76a6ec9ca94dcb6b07a2","file_size":2248814,"date_updated":"2020-07-14T12:47:38Z","creator":"system","file_name":"IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf","date_created":"2018-12-12T10:14:54Z"}],"publication_status":"published","publication_identifier":{"issn":["22111247"]}},{"title":"Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6","publist_id":"7050","author":[{"first_name":"Jan","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","last_name":"Schwarz","full_name":"Schwarz, Jan"},{"last_name":"Bierbaum","full_name":"Bierbaum, Veronika","first_name":"Veronika","id":"3FD04378-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Kari","id":"368EE576-F248-11E8-B48F-1D18A9856A87","full_name":"Vaahtomeri, Kari","orcid":"0000-0001-7829-3518","last_name":"Vaahtomeri"},{"last_name":"Hauschild","full_name":"Hauschild, Robert","orcid":"0000-0001-9843-3522","first_name":"Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Brown, Markus","last_name":"Brown","first_name":"Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","last_name":"De Vries","full_name":"De Vries, Ingrid"},{"full_name":"Leithner, Alexander F","last_name":"Leithner","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander F"},{"first_name":"Anne","id":"35B76592-F248-11E8-B48F-1D18A9856A87","last_name":"Reversat","orcid":"0000-0003-0666-8928","full_name":"Reversat, Anne"},{"orcid":"0000-0001-5145-4609","full_name":"Merrin, Jack","last_name":"Merrin","first_name":"Jack","id":"4515C308-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Tarrant, Teresa","last_name":"Tarrant","first_name":"Teresa"},{"last_name":"Bollenbach","full_name":"Bollenbach, Tobias","orcid":"0000-0003-4398-476X","first_name":"Tobias","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt"}],"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Schwarz, Jan, Veronika Bierbaum, Kari Vaahtomeri, Robert Hauschild, Markus Brown, Ingrid de Vries, Alexander F Leithner, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2017.04.004.","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.","mla":"Schwarz, Jan, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current Biology, vol. 27, no. 9, Cell Press, 2017, pp. 1314–25, doi:10.1016/j.cub.2017.04.004.","apa":"Schwarz, J., Bierbaum, V., Vaahtomeri, K., Hauschild, R., Brown, M., de Vries, I., … Sixt, M. K. (2017). Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2017.04.004","ama":"Schwarz J, Bierbaum V, Vaahtomeri K, et al. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. 2017;27(9):1314-1325. doi:10.1016/j.cub.2017.04.004","ieee":"J. Schwarz et al., “Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6,” Current Biology, vol. 27, no. 9. Cell Press, pp. 1314–1325, 2017.","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."},"project":[{"name":"International IST Postdoc Fellowship Programme","grant_number":"291734","call_identifier":"FP7","_id":"25681D80-B435-11E9-9278-68D0E5697425"},{"_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12"}],"date_created":"2018-12-11T11:47:51Z","date_published":"2017-05-09T00:00:00Z","doi":"10.1016/j.cub.2017.04.004","page":"1314 - 1325","publication":"Current Biology","day":"09","year":"2017","quality_controlled":"1","publisher":"Cell Press","department":[{"_id":"MiSi"},{"_id":"Bio"},{"_id":"NanoFab"}],"date_updated":"2023-02-23T12:50:44Z","status":"public","type":"journal_article","_id":"674","ec_funded":1,"volume":27,"issue":"9","language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"issn":["09609822"]},"intvolume":" 27","month":"05","scopus_import":1,"oa_version":"None","abstract":[{"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.","lang":"eng"}]},{"status":"public","pubrep_id":"899","type":"journal_article","tmp":{"short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","image":"/images/cc_by_nc_nd.png"},"_id":"677","department":[{"_id":"MiSi"}],"file_date_updated":"2020-07-14T12:47:40Z","ddc":["570"],"date_updated":"2021-01-12T08:08:57Z","month":"05","intvolume":" 19","scopus_import":1,"oa_version":"Published Version","abstract":[{"lang":"eng","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."}],"issue":"7","volume":19,"file":[{"creator":"system","file_size":3005610,"date_updated":"2020-07-14T12:47:40Z","file_name":"IST-2017-899-v1+1_1-s2.0-S2211124717305454-main.pdf","date_created":"2018-12-12T10:15:48Z","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_id":"5171","checksum":"efc7287d9c6354983cb151880e9ad72a"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["22111247"]},"publication_status":"published","title":"The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination","publist_id":"7046","author":[{"first_name":"Claudio","last_name":"Lademann","full_name":"Lademann, Claudio"},{"first_name":"Jörg","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","last_name":"Renkawitz","orcid":"0000-0003-2856-3369","full_name":"Renkawitz, Jörg"},{"first_name":"Boris","last_name":"Pfander","full_name":"Pfander, Boris"},{"full_name":"Jentsch, Stefan","last_name":"Jentsch","first_name":"Stefan"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"Lademann, Claudio, et al. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” Cell Reports, vol. 19, no. 7, Cell Press, 2017, pp. 1294–303, doi:10.1016/j.celrep.2017.04.051.","short":"C. Lademann, J. Renkawitz, B. Pfander, S. Jentsch, Cell Reports 19 (2017) 1294–1303.","ieee":"C. Lademann, J. Renkawitz, B. Pfander, and S. Jentsch, “The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination,” Cell Reports, vol. 19, no. 7. Cell Press, pp. 1294–1303, 2017.","apa":"Lademann, C., Renkawitz, J., Pfander, B., & Jentsch, S. (2017). The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.051","ama":"Lademann C, Renkawitz J, Pfander B, Jentsch S. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. 2017;19(7):1294-1303. doi:10.1016/j.celrep.2017.04.051","chicago":"Lademann, Claudio, Jörg Renkawitz, Boris Pfander, and Stefan Jentsch. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.051.","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."},"publisher":"Cell Press","quality_controlled":"1","oa":1,"date_published":"2017-05-16T00:00:00Z","doi":"10.1016/j.celrep.2017.04.051","date_created":"2018-12-11T11:47:52Z","page":"1294 - 1303","day":"16","publication":"Cell Reports","has_accepted_license":"1","year":"2017"},{"publisher":"Company of Biologists","quality_controlled":"1","oa":1,"page":"2172 - 2184","date_published":"2017-07-01T00:00:00Z","doi":"10.1242/jcs.200899","date_created":"2018-12-11T11:47:58Z","has_accepted_license":"1","year":"2017","day":"01","publication":"Journal of Cell Science","publist_id":"7008","author":[{"full_name":"Veß, Astrid","last_name":"Veß","first_name":"Astrid"},{"last_name":"Blache","full_name":"Blache, Ulrich","first_name":"Ulrich"},{"full_name":"Leitner, Laura","last_name":"Leitner","first_name":"Laura"},{"first_name":"Angela","last_name":"Kurz","full_name":"Kurz, Angela"},{"first_name":"Anja","full_name":"Ehrenpfordt, Anja","last_name":"Ehrenpfordt"},{"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":"Posern, Guido","last_name":"Posern","first_name":"Guido"}],"external_id":{"pmid":["28515231"]},"title":"A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity","citation":{"short":"A. Veß, U. Blache, L. Leitner, A. Kurz, A. Ehrenpfordt, M.K. Sixt, G. Posern, Journal of Cell Science 130 (2017) 2172–2184.","ieee":"A. Veß et al., “A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity,” Journal of Cell Science, vol. 130, no. 13. Company of Biologists, pp. 2172–2184, 2017.","apa":"Veß, A., Blache, U., Leitner, L., Kurz, A., Ehrenpfordt, A., Sixt, M. K., & Posern, G. (2017). A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.200899","ama":"Veß A, Blache U, Leitner L, et al. A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. 2017;130(13):2172-2184. doi:10.1242/jcs.200899","mla":"Veß, Astrid, et al. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell Science, vol. 130, no. 13, Company of Biologists, 2017, pp. 2172–84, doi:10.1242/jcs.200899.","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.","chicago":"Veß, Astrid, Ulrich Blache, Laura Leitner, Angela Kurz, Anja Ehrenpfordt, Michael K Sixt, and Guido Posern. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell Science. Company of Biologists, 2017. https://doi.org/10.1242/jcs.200899."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","scopus_import":1,"month":"07","intvolume":" 130","abstract":[{"text":"A change regarding the extent of adhesion - hereafter referred to as adhesion plasticity - between adhesive and less-adhesive states of mammalian cells is important for their behavior. To investigate adhesion plasticity, we have selected a stable isogenic subpopulation of human MDA-MB-468 breast carcinoma cells growing in suspension. These suspension cells are unable to re-adhere to various matrices or to contract three-dimensional collagen lattices. By using transcriptome analysis, we identified the focal adhesion protein tensin3 (Tns3) as a determinant of adhesion plasticity. Tns3 is strongly reduced at mRNA and protein levels in suspension cells. Furthermore, by transiently challenging breast cancer cells to grow under non-adherent conditions markedly reduces Tns3 protein expression, which is regained upon re-adhesion. Stable knockdown of Tns3 in parental MDA-MB-468 cells results in defective adhesion, spreading and migration. Tns3-knockdown cells display impaired structure and dynamics of focal adhesion complexes as determined by immunostaining. Restoration of Tns3 protein expression in suspension cells partially rescues adhesion and focal contact composition. Our work identifies Tns3 as a crucial focal adhesion component regulated by, and functionally contributing to, the switch between adhesive and non-adhesive states in MDA-MB-468 cancer cells.","lang":"eng"}],"pmid":1,"oa_version":"Published Version","volume":130,"issue":"13","publication_identifier":{"issn":["00219533"]},"publication_status":"published","file":[{"date_created":"2019-10-24T09:43:56Z","file_name":"2017_CellScience_Vess.pdf","creator":"dernst","date_updated":"2020-07-14T12:47:45Z","file_size":10847596,"file_id":"6966","checksum":"42c81a0a4fc3128883b391c3af3f74bc","access_level":"open_access","relation":"main_file","content_type":"application/pdf"}],"language":[{"iso":"eng"}],"type":"journal_article","article_type":"original","status":"public","_id":"694","department":[{"_id":"MiSi"}],"file_date_updated":"2020-07-14T12:47:45Z","date_updated":"2021-01-12T08:09:41Z","ddc":["570"]},{"quality_controlled":"1","publisher":"Cell Press","page":"R24 - R25","date_created":"2018-12-11T11:50:29Z","date_published":"2017-01-09T00:00:00Z","doi":"10.1016/j.cub.2016.11.035","year":"2017","isi":1,"publication":"Current Biology","day":"09","external_id":{"isi":["000391902500010"]},"article_processing_charge":"No","publist_id":"6197","author":[{"first_name":"Jan","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D","last_name":"Müller","full_name":"Müller, Jan"},{"last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"title":"Cell migration: Making the waves","citation":{"ista":"Müller J, Sixt MK. 2017. Cell migration: Making the waves. Current Biology. 27(1), R24–R25.","chicago":"Müller, Jan, and Michael K Sixt. “Cell Migration: Making the Waves.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2016.11.035.","ieee":"J. Müller and M. K. Sixt, “Cell migration: Making the waves,” Current Biology, vol. 27, no. 1. Cell Press, pp. R24–R25, 2017.","short":"J. Müller, M.K. Sixt, Current Biology 27 (2017) R24–R25.","apa":"Müller, J., & Sixt, M. K. (2017). Cell migration: Making the waves. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2016.11.035","ama":"Müller J, Sixt MK. Cell migration: Making the waves. Current Biology. 2017;27(1):R24-R25. doi:10.1016/j.cub.2016.11.035","mla":"Müller, Jan, and Michael K. Sixt. “Cell Migration: Making the Waves.” Current Biology, vol. 27, no. 1, Cell Press, 2017, pp. R24–25, doi:10.1016/j.cub.2016.11.035."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","scopus_import":"1","intvolume":" 27","month":"01","abstract":[{"lang":"eng","text":"Coordinated changes of cell shape are often the result of the excitable, wave-like dynamics of the actin cytoskeleton. New work shows that, in migrating cells, protrusion waves arise from mechanochemical crosstalk between adhesion sites, membrane tension and the actin protrusive machinery."}],"oa_version":"None","volume":27,"issue":"1","publication_status":"published","publication_identifier":{"issn":["09609822"]},"language":[{"iso":"eng"}],"type":"journal_article","status":"public","_id":"1161","department":[{"_id":"MiSi"}],"date_updated":"2023-09-20T11:28:19Z"}]