[{"has_accepted_license":"1","status":"public","isi":1,"ddc":["570"],"language":[{"iso":"eng"}],"file":[{"file_id":"5973","access_level":"open_access","file_size":358141,"date_created":"2019-02-13T10:52:11Z","date_updated":"2020-07-14T12:47:13Z","relation":"main_file","creator":"dernst","file_name":"2018_eLife_Alanko.pdf","checksum":"f1c7ec2a809408d763c4b529a98f9a3b","content_type":"application/pdf"}],"date_created":"2019-01-20T22:59:19Z","date_updated":"2025-07-10T11:53:05Z","article_processing_charge":"No","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","month":"06","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"citation":{"chicago":"Alanko, Jonna H, and Michael K Sixt. “The Cell Sets the Tone.” <i>ELife</i>. eLife Sciences Publications, 2018. <a href=\"https://doi.org/10.7554/eLife.37888\">https://doi.org/10.7554/eLife.37888</a>.","apa":"Alanko, J. H., &#38; Sixt, M. K. (2018). The cell sets the tone. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/eLife.37888\">https://doi.org/10.7554/eLife.37888</a>","ieee":"J. H. Alanko and M. K. Sixt, “The cell sets the tone,” <i>eLife</i>, vol. 7. eLife Sciences Publications, 2018.","ama":"Alanko JH, Sixt MK. The cell sets the tone. <i>eLife</i>. 2018;7. doi:<a href=\"https://doi.org/10.7554/eLife.37888\">10.7554/eLife.37888</a>","short":"J.H. Alanko, M.K. Sixt, ELife 7 (2018).","ista":"Alanko JH, Sixt MK. 2018. The cell sets the tone. eLife. 7, e37888.","mla":"Alanko, Jonna H., and Michael K. Sixt. “The Cell Sets the Tone.” <i>ELife</i>, vol. 7, e37888, eLife Sciences Publications, 2018, doi:<a href=\"https://doi.org/10.7554/eLife.37888\">10.7554/eLife.37888</a>."},"oa_version":"Published Version","author":[{"last_name":"Alanko","id":"2CC12E8C-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7698-3061","full_name":"Alanko, Jonna H","first_name":"Jonna H"},{"full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"}],"type":"journal_article","publication_status":"published","quality_controlled":"1","file_date_updated":"2020-07-14T12:47:13Z","year":"2018","doi":"10.7554/eLife.37888","fulldoi":"https://doi.org/10.7554/eLife.37888","day":"06","abstract":[{"lang":"eng","text":"In zebrafish larvae, it is the cell type that determines how the cell responds to a chemokine signal."}],"volume":7,"publication":"eLife","external_id":{"isi":["000434375000001"]},"publisher":"eLife Sciences Publications","department":[{"_id":"MiSi"}],"oa":1,"corr_author":"1","publication_identifier":{"issn":["2050-084X"]},"_id":"5861","title":"The cell sets the tone","scopus_import":"1","article_number":"e37888","intvolume":"         7","date_published":"2018-06-06T00:00:00Z","article_type":"original"},{"issue":"1","isi":1,"language":[{"iso":"eng"}],"ddc":["570"],"status":"public","has_accepted_license":"1","date_updated":"2025-04-15T07:22:42Z","date_created":"2019-02-14T10:50:24Z","file":[{"access_level":"open_access","file_size":1349914,"file_id":"5985","checksum":"8325fcc194264af4749e662a73bf66b5","content_type":"application/pdf","relation":"main_file","date_created":"2019-02-14T10:58:29Z","date_updated":"2020-07-14T12:47:14Z","creator":"kschuh","file_name":"2018_Springer_Morri.pdf"}],"month":"12","citation":{"mla":"Morri, Maurizio, et al. “Optical Functionalization of Human Class A Orphan G-Protein-Coupled Receptors.” <i>Nature Communications</i>, vol. 9, no. 1, 1950, Springer Nature, 2018, doi:<a href=\"https://doi.org/10.1038/s41467-018-04342-1\">10.1038/s41467-018-04342-1</a>.","ista":"Morri M, Sanchez-Romero I, Tichy A-M, Kainrath S, Gerrard EJ, Hirschfeld P, Schwarz J, Janovjak HL. 2018. Optical functionalization of human class A orphan G-protein-coupled receptors. Nature Communications. 9(1), 1950.","short":"M. Morri, I. Sanchez-Romero, A.-M. Tichy, S. Kainrath, E.J. Gerrard, P. Hirschfeld, J. Schwarz, H.L. Janovjak, Nature Communications 9 (2018).","ama":"Morri M, Sanchez-Romero I, Tichy A-M, et al. Optical functionalization of human class A orphan G-protein-coupled receptors. <i>Nature Communications</i>. 2018;9(1). doi:<a href=\"https://doi.org/10.1038/s41467-018-04342-1\">10.1038/s41467-018-04342-1</a>","apa":"Morri, M., Sanchez-Romero, I., Tichy, A.-M., Kainrath, S., Gerrard, E. J., Hirschfeld, P., … Janovjak, H. L. (2018). Optical functionalization of human class A orphan G-protein-coupled receptors. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-018-04342-1\">https://doi.org/10.1038/s41467-018-04342-1</a>","ieee":"M. Morri <i>et al.</i>, “Optical functionalization of human class A orphan G-protein-coupled receptors,” <i>Nature Communications</i>, vol. 9, no. 1. Springer Nature, 2018.","chicago":"Morri, Maurizio, Inmaculada Sanchez-Romero, Alexandra-Madelaine Tichy, Stephanie Kainrath, Elliot J. Gerrard, Priscila Hirschfeld, Jan Schwarz, and Harald L Janovjak. “Optical Functionalization of Human Class A Orphan G-Protein-Coupled Receptors.” <i>Nature Communications</i>. Springer Nature, 2018. <a href=\"https://doi.org/10.1038/s41467-018-04342-1\">https://doi.org/10.1038/s41467-018-04342-1</a>."},"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"oa_version":"Published Version","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","article_processing_charge":"No","quality_controlled":"1","file_date_updated":"2020-07-14T12:47:14Z","type":"journal_article","author":[{"full_name":"Morri, Maurizio","first_name":"Maurizio","last_name":"Morri","id":"4863116E-F248-11E8-B48F-1D18A9856A87"},{"id":"3D9C5D30-F248-11E8-B48F-1D18A9856A87","last_name":"Sanchez-Romero","first_name":"Inmaculada","full_name":"Sanchez-Romero, Inmaculada"},{"id":"29D8BB2C-F248-11E8-B48F-1D18A9856A87","last_name":"Tichy","first_name":"Alexandra-Madelaine","full_name":"Tichy, Alexandra-Madelaine"},{"first_name":"Stephanie","full_name":"Kainrath, Stephanie","id":"32CFBA64-F248-11E8-B48F-1D18A9856A87","last_name":"Kainrath"},{"last_name":"Gerrard","first_name":"Elliot J.","full_name":"Gerrard, Elliot J."},{"last_name":"Hirschfeld","id":"435ACB3A-F248-11E8-B48F-1D18A9856A87","full_name":"Hirschfeld, Priscila","first_name":"Priscila"},{"first_name":"Jan","full_name":"Schwarz, Jan","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","last_name":"Schwarz"},{"orcid":"0000-0002-8023-9315","id":"33BA6C30-F248-11E8-B48F-1D18A9856A87","last_name":"Janovjak","first_name":"Harald L","full_name":"Janovjak, Harald L"}],"publication_status":"published","abstract":[{"lang":"eng","text":"G-protein-coupled receptors (GPCRs) form the largest receptor family, relay environmental stimuli to changes in cell behavior and represent prime drug targets. Many GPCRs are classified as orphan receptors because of the limited knowledge on their ligands and coupling to cellular signaling machineries. Here, we engineer a library of 63 chimeric receptors that contain the signaling domains of human orphan and understudied GPCRs functionally linked to the light-sensing domain of rhodopsin. Upon stimulation with visible light, we identify activation of canonical cell signaling pathways, including cAMP-, Ca2+-, MAPK/ERK-, and Rho-dependent pathways, downstream of the engineered receptors. For the human pseudogene GPR33, we resurrect a signaling function that supports its hypothesized role as a pathogen entry site. These results demonstrate that substituting unknown chemical activators with a light switch can reveal information about protein function and provide an optically controlled protein library for exploring the physiology and therapeutic potential of understudied GPCRs."}],"ec_funded":1,"project":[{"_id":"25548C20-B435-11E9-9278-68D0E5697425","name":"Microbial Ion Channels for Synthetic Neurobiology","grant_number":"303564","call_identifier":"FP7"},{"_id":"255A6082-B435-11E9-9278-68D0E5697425","name":"Molecular Drug Targets","grant_number":"W1232-B24","call_identifier":"FWF"}],"volume":9,"doi":"10.1038/s41467-018-04342-1","year":"2018","day":"01","fulldoi":"https://doi.org/10.1038/s41467-018-04342-1","publisher":"Springer Nature","external_id":{"isi":["000432280000006"]},"publication":"Nature Communications","_id":"5984","oa":1,"department":[{"_id":"HaJa"},{"_id":"CaGu"},{"_id":"MiSi"}],"publication_identifier":{"issn":["2041-1723"]},"date_published":"2018-12-01T00:00:00Z","article_number":"1950","intvolume":"         9","scopus_import":"1","title":"Optical functionalization of human class A orphan G-protein-coupled receptors"},{"issue":"18","ddc":["570"],"language":[{"iso":"eng"}],"OA_place":"publisher","has_accepted_license":"1","status":"public","date_updated":"2025-05-20T07:43:06Z","date_created":"2019-04-29T09:40:33Z","file":[{"file_id":"6360","file_size":2928337,"access_level":"open_access","creator":"dernst","file_name":"2018_BioProtocol_Fan.pdf","relation":"main_file","date_created":"2019-04-30T08:04:33Z","date_updated":"2020-07-14T12:47:28Z","content_type":"application/pdf","checksum":"d4588377e789da7f360b553ae02c5119"}],"month":"09","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"citation":{"ista":"Fan S, Lorenz M, Massberg S, Gärtner FR. 2018. Platelet migration and bacterial trapping assay under flow. Bio-Protocol. 8(18), e3018.","short":"S. Fan, M. Lorenz, S. Massberg, F.R. Gärtner, Bio-Protocol 8 (2018).","mla":"Fan, Shuxia, et al. “Platelet Migration and Bacterial Trapping Assay under Flow.” <i>Bio-Protocol</i>, vol. 8, no. 18, e3018, Bio-Protocol, 2018, doi:<a href=\"https://doi.org/10.21769/bioprotoc.3018\">10.21769/bioprotoc.3018</a>.","chicago":"Fan, Shuxia, Michael Lorenz, Steffen Massberg, and Florian R Gärtner. “Platelet Migration and Bacterial Trapping Assay under Flow.” <i>Bio-Protocol</i>. Bio-Protocol, 2018. <a href=\"https://doi.org/10.21769/bioprotoc.3018\">https://doi.org/10.21769/bioprotoc.3018</a>.","apa":"Fan, S., Lorenz, M., Massberg, S., &#38; Gärtner, F. R. (2018). Platelet migration and bacterial trapping assay under flow. <i>Bio-Protocol</i>. Bio-Protocol. <a href=\"https://doi.org/10.21769/bioprotoc.3018\">https://doi.org/10.21769/bioprotoc.3018</a>","ieee":"S. Fan, M. Lorenz, S. Massberg, and F. R. Gärtner, “Platelet migration and bacterial trapping assay under flow,” <i>Bio-Protocol</i>, vol. 8, no. 18. Bio-Protocol, 2018.","ama":"Fan S, Lorenz M, Massberg S, Gärtner FR. Platelet migration and bacterial trapping assay under flow. <i>Bio-Protocol</i>. 2018;8(18). doi:<a href=\"https://doi.org/10.21769/bioprotoc.3018\">10.21769/bioprotoc.3018</a>"},"oa_version":"Published Version","DOAJ_listed":"1","article_processing_charge":"Yes","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","quality_controlled":"1","file_date_updated":"2020-07-14T12:47:28Z","author":[{"first_name":"Shuxia","full_name":"Fan, Shuxia","last_name":"Fan"},{"full_name":"Lorenz, Michael","first_name":"Michael","last_name":"Lorenz"},{"last_name":"Massberg","full_name":"Massberg, Steffen","first_name":"Steffen"},{"full_name":"Gärtner, Florian R","first_name":"Florian R","last_name":"Gärtner","id":"397A88EE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6120-3723"}],"type":"journal_article","publication_status":"published","abstract":[{"lang":"eng","text":"Blood platelets are critical for hemostasis and thrombosis, but also play diverse roles during immune responses. We have recently reported that platelets migrate at sites of infection in vitro and in vivo. Importantly, platelets use their ability to migrate to collect and bundle fibrin (ogen)-bound bacteria accomplishing efficient intravascular bacterial trapping. Here, we describe a method that allows analyzing platelet migration in vitro, focusing on their ability to collect bacteria and trap bacteria under flow."}],"ec_funded":1,"volume":8,"project":[{"grant_number":"747687","call_identifier":"H2020","_id":"260AA4E2-B435-11E9-9278-68D0E5697425","name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells"}],"year":"2018","doi":"10.21769/bioprotoc.3018","keyword":["Platelets","Cell migration","Bacteria","Shear flow","Fibrinogen","E. coli"],"fulldoi":"https://doi.org/10.21769/bioprotoc.3018","acknowledgement":"This protocol was adapted from a previously published study (Gaertner et al., 2017). We thank Michael Lorenz for his excellent assistance in bacteria culture. This work was funded by the DFG SFB 914 (S.M. [B02 and Z01]), the DFG SFB 1123 (S.M. [B06]), the DFG FOR 2033 (S.M. and F.G.), the German Centre for Cardiovascular Research (DZHK) (MHA 1.4VD [S.M.]), FP7 program (project 260309, PRESTIGE [S.M.]), FöFoLe project 947 (F.G.), the Friedrich-Baur-Stiftung project 41/16 (F.G.), Marie Sklodowska Curie Individual Fellowship (EU project 747687, LamelliaActin [F.G.]).","day":"20","OA_type":"gold","pmid":1,"external_id":{"pmid":["34395806"]},"publication":"Bio-Protocol","publisher":"Bio-Protocol","_id":"6354","department":[{"_id":"MiSi"}],"oa":1,"corr_author":"1","publication_identifier":{"issn":["2331-8325"]},"date_published":"2018-09-20T00:00:00Z","article_type":"original","title":"Platelet migration and bacterial trapping assay under flow","intvolume":"         8","article_number":"e3018"},{"publication_status":"published","type":"journal_article","author":[{"last_name":"Moalli","first_name":"Federica","full_name":"Moalli, Federica"},{"last_name":"Ficht","first_name":"Xenia","full_name":"Ficht, Xenia"},{"full_name":"Germann, Philipp","first_name":"Philipp","last_name":"Germann"},{"last_name":"Vladymyrov","first_name":"Mykhailo","full_name":"Vladymyrov, Mykhailo"},{"last_name":"Stolp","first_name":"Bettina","full_name":"Stolp, Bettina"},{"id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","last_name":"de Vries","first_name":"Ingrid","full_name":"de Vries, Ingrid"},{"first_name":"Ruth","full_name":"Lyck, Ruth","last_name":"Lyck"},{"last_name":"Balmer","full_name":"Balmer, Jasmin","first_name":"Jasmin"},{"last_name":"Fiocchi","first_name":"Amleto","full_name":"Fiocchi, Amleto"},{"full_name":"Kreutzfeldt, Mario","first_name":"Mario","last_name":"Kreutzfeldt"},{"last_name":"Merkler","first_name":"Doron","full_name":"Merkler, Doron"},{"last_name":"Iannacone","first_name":"Matteo","full_name":"Iannacone, Matteo"},{"last_name":"Ariga","first_name":"Akitaka","full_name":"Ariga, Akitaka"},{"last_name":"Stoffel","full_name":"Stoffel, Michael H.","first_name":"Michael H."},{"last_name":"Sharpe","first_name":"James","full_name":"Sharpe, James"},{"first_name":"Martin","full_name":"Bähler, Martin","last_name":"Bähler"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","orcid":"0000-0002-6620-9179","first_name":"Michael K","full_name":"Sixt, Michael K"},{"last_name":"Diz-Muñoz","full_name":"Diz-Muñoz, Alba","first_name":"Alba"},{"last_name":"Stein","full_name":"Stein, Jens V.","first_name":"Jens V."}],"file_date_updated":"2020-07-14T12:47:32Z","quality_controlled":"1","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","article_processing_charge":"No","tmp":{"name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","image":"/images/cc_by_nc_sa.png","short":"CC BY-NC-SA (4.0)"},"citation":{"apa":"Moalli, F., Ficht, X., Germann, P., Vladymyrov, M., Stolp, B., de Vries, I., … Stein, J. V. (2018). The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. <i>The Journal of Experimental Medicine</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1084/jem.20170896\">https://doi.org/10.1084/jem.20170896</a>","ieee":"F. Moalli <i>et al.</i>, “The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells,” <i>The Journal of Experimental Medicine</i>, vol. 2015, no. 7. Rockefeller University Press, pp. 1869–1890, 2018.","ama":"Moalli F, Ficht X, Germann P, et al. The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. <i>The Journal of Experimental Medicine</i>. 2018;2015(7):1869–1890. doi:<a href=\"https://doi.org/10.1084/jem.20170896\">10.1084/jem.20170896</a>","chicago":"Moalli, Federica, Xenia Ficht, Philipp Germann, Mykhailo Vladymyrov, Bettina Stolp, Ingrid de Vries, Ruth Lyck, et al. “The Rho Regulator Myosin IXb Enables Nonlymphoid Tissue Seeding of Protective CD8+T Cells.” <i>The Journal of Experimental Medicine</i>. Rockefeller University Press, 2018. <a href=\"https://doi.org/10.1084/jem.20170896\">https://doi.org/10.1084/jem.20170896</a>.","mla":"Moalli, Federica, et al. “The Rho Regulator Myosin IXb Enables Nonlymphoid Tissue Seeding of Protective CD8+T Cells.” <i>The Journal of Experimental Medicine</i>, vol. 2015, no. 7, Rockefeller University Press, 2018, pp. 1869–1890, doi:<a href=\"https://doi.org/10.1084/jem.20170896\">10.1084/jem.20170896</a>.","ista":"Moalli F, Ficht X, Germann P, Vladymyrov M, Stolp B, de Vries I, Lyck R, Balmer J, Fiocchi A, Kreutzfeldt M, Merkler D, Iannacone M, Ariga A, Stoffel MH, Sharpe J, Bähler M, Sixt MK, Diz-Muñoz A, Stein JV. 2018. The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. The Journal of Experimental Medicine. 2015(7), 1869–1890.","short":"F. Moalli, X. Ficht, P. Germann, M. Vladymyrov, B. Stolp, I. de Vries, R. Lyck, J. Balmer, A. Fiocchi, M. Kreutzfeldt, D. Merkler, M. Iannacone, A. Ariga, M.H. Stoffel, J. Sharpe, M. Bähler, M.K. Sixt, A. Diz-Muñoz, J.V. Stein, The Journal of Experimental Medicine 2015 (2018) 1869–1890."},"oa_version":"Published Version","month":"06","file":[{"content_type":"application/pdf","checksum":"86ae5331f9bfced9a6358a790a04bef4","creator":"kschuh","file_name":"2018_rupress_Moalli.pdf","date_created":"2019-05-28T12:40:05Z","date_updated":"2020-07-14T12:47:32Z","relation":"main_file","access_level":"open_access","file_size":3841660,"file_id":"6498"}],"date_created":"2019-05-28T12:36:47Z","date_updated":"2023-09-19T14:52:08Z","status":"public","has_accepted_license":"1","ddc":["570"],"language":[{"iso":"eng"}],"isi":1,"issue":"7","license":"https://creativecommons.org/licenses/by-nc-sa/4.0/","intvolume":"      2015","scopus_import":"1","title":"The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells","date_published":"2018-06-06T00:00:00Z","publication_identifier":{"eissn":["1540-9538"],"issn":["0022-1007"]},"department":[{"_id":"MiSi"}],"oa":1,"_id":"6497","publisher":"Rockefeller University Press","page":"1869–1890","publication":"The Journal of Experimental Medicine","external_id":{"isi":["000440822900011"]},"day":"06","fulldoi":"https://doi.org/10.1084/jem.20170896","doi":"10.1084/jem.20170896","year":"2018","volume":2015,"abstract":[{"lang":"eng","text":"T cells are actively scanning pMHC-presenting cells in lymphoid organs and nonlymphoid tissues (NLTs) with divergent topologies and confinement. How the T cell actomyosin cytoskeleton facilitates this task in distinct environments is incompletely understood. Here, we show that lack of Myosin IXb (Myo9b), a negative regulator of the small GTPase Rho, led to increased Rho-GTP levels and cell surface stiffness in primary T cells. Nonetheless, intravital imaging revealed robust motility of Myo9b−/− CD8+ T cells in lymphoid tissue and similar expansion and differentiation during immune responses. In contrast, accumulation of Myo9b−/− CD8+ T cells in NLTs was strongly impaired. Specifically, Myo9b was required for T cell crossing of basement membranes, such as those which are present between dermis and epidermis. As consequence, Myo9b−/− CD8+ T cells showed impaired control of skin infections. In sum, we show that Myo9b is critical for the CD8+ T cell adaptation from lymphoid to NLT surveillance and the establishment of protective tissue–resident T cell populations."}]},{"_id":"318","corr_author":"1","oa":1,"department":[{"_id":"MiSi"}],"date_published":"2018-02-26T00:00:00Z","scopus_import":"1","title":"A fat lot of good for wound healing","intvolume":"        44","volume":44,"abstract":[{"text":"The insect’s fat body combines metabolic and immunological functions. In this issue of Developmental Cell, Franz et al. (2018) show that in Drosophila, cells of the fat body are not static, but can actively “swim” toward sites of epithelial injury, where they physically clog the wound and locally secrete antimicrobial peptides.","lang":"eng"}],"fulldoi":"https://doi.org/10.1016/j.devcel.2018.02.009","acknowledgement":"Short Survey","day":"26","year":"2018","doi":"10.1016/j.devcel.2018.02.009","publication":"Developmental Cell","page":"405 - 406","external_id":{"pmid":["29486189"],"isi":["000426150700002"]},"publisher":"Cell Press","pmid":1,"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pubmed/29486189","open_access":"1"}],"oa_version":"Published Version","citation":{"ista":"Casano AM, Sixt MK. 2018. A fat lot of good for wound healing. Developmental Cell. 44(4), 405–406.","short":"A.M. Casano, M.K. Sixt, Developmental Cell 44 (2018) 405–406.","mla":"Casano, Alessandra M., and Michael K. Sixt. “A Fat Lot of Good for Wound Healing.” <i>Developmental Cell</i>, vol. 44, no. 4, Cell Press, 2018, pp. 405–06, doi:<a href=\"https://doi.org/10.1016/j.devcel.2018.02.009\">10.1016/j.devcel.2018.02.009</a>.","chicago":"Casano, Alessandra M, and Michael K Sixt. “A Fat Lot of Good for Wound Healing.” <i>Developmental Cell</i>. Cell Press, 2018. <a href=\"https://doi.org/10.1016/j.devcel.2018.02.009\">https://doi.org/10.1016/j.devcel.2018.02.009</a>.","ama":"Casano AM, Sixt MK. A fat lot of good for wound healing. <i>Developmental Cell</i>. 2018;44(4):405-406. doi:<a href=\"https://doi.org/10.1016/j.devcel.2018.02.009\">10.1016/j.devcel.2018.02.009</a>","ieee":"A. M. Casano and M. K. Sixt, “A fat lot of good for wound healing,” <i>Developmental Cell</i>, vol. 44, no. 4. Cell Press, pp. 405–406, 2018.","apa":"Casano, A. M., &#38; Sixt, M. K. (2018). A fat lot of good for wound healing. <i>Developmental Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.devcel.2018.02.009\">https://doi.org/10.1016/j.devcel.2018.02.009</a>"},"month":"02","article_processing_charge":"No","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","quality_controlled":"1","publication_status":"published","author":[{"orcid":"0000-0002-6009-6804","id":"3DBA3F4E-F248-11E8-B48F-1D18A9856A87","last_name":"Casano","first_name":"Alessandra M","full_name":"Casano, Alessandra M"},{"first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt"}],"type":"journal_article","ddc":["570"],"language":[{"iso":"eng"}],"issue":"4","isi":1,"status":"public","publist_id":"7547","date_created":"2018-12-11T11:45:47Z","date_updated":"2026-06-18T18:39:56Z"},{"status":"public","has_accepted_license":"1","ddc":["570"],"language":[{"iso":"eng"}],"isi":1,"issue":"22","file":[{"file_size":6668971,"access_level":"open_access","file_id":"5994","content_type":"application/pdf","checksum":"e98465b4416b3e804c47f40086932af2","file_name":"2018_ASCB_Dolati.pdf","creator":"kschuh","relation":"main_file","date_created":"2019-02-14T12:34:29Z","date_updated":"2020-07-14T12:47:15Z"}],"date_updated":"2026-07-06T12:25:34Z","date_created":"2019-02-14T12:25:47Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","tmp":{"name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","image":"/images/cc_by_nc_sa.png","short":"CC BY-NC-SA (4.0)"},"oa_version":"Published Version","citation":{"ieee":"S. Dolati <i>et al.</i>, “On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility,” <i>Molecular Biology of the Cell</i>, vol. 29, no. 22. American Society for Cell Biology, pp. 2674–2686, 2018.","apa":"Dolati, S., Kage, F., Mueller, J., Müsken, M., Kirchner, M., Dittmar, G., … Falcke, M. (2018). On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility. <i>Molecular Biology of the Cell</i>. American Society for Cell Biology. <a href=\"https://doi.org/10.1091/mbc.e18-02-0082\">https://doi.org/10.1091/mbc.e18-02-0082</a>","ama":"Dolati S, Kage F, Mueller J, et al. On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility. <i>Molecular Biology of the Cell</i>. 2018;29(22):2674-2686. doi:<a href=\"https://doi.org/10.1091/mbc.e18-02-0082\">10.1091/mbc.e18-02-0082</a>","chicago":"Dolati, Setareh, Frieda Kage, Jan Mueller, Mathias Müsken, Marieluise Kirchner, Gunnar Dittmar, Michael K Sixt, Klemens Rottner, and Martin Falcke. “On the Relation between Filament Density, Force Generation, and Protrusion Rate in Mesenchymal Cell Motility.” <i>Molecular Biology of the Cell</i>. American Society for Cell Biology, 2018. <a href=\"https://doi.org/10.1091/mbc.e18-02-0082\">https://doi.org/10.1091/mbc.e18-02-0082</a>.","mla":"Dolati, Setareh, et al. “On the Relation between Filament Density, Force Generation, and Protrusion Rate in Mesenchymal Cell Motility.” <i>Molecular Biology of the Cell</i>, vol. 29, no. 22, American Society for Cell Biology, 2018, pp. 2674–86, doi:<a href=\"https://doi.org/10.1091/mbc.e18-02-0082\">10.1091/mbc.e18-02-0082</a>.","short":"S. Dolati, F. Kage, J. Mueller, M. Müsken, M. Kirchner, G. Dittmar, M.K. Sixt, K. Rottner, M. Falcke, Molecular Biology of the Cell 29 (2018) 2674–2686.","ista":"Dolati S, Kage F, Mueller J, Müsken M, Kirchner M, Dittmar G, Sixt MK, Rottner K, Falcke M. 2018. On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility. Molecular Biology of the Cell. 29(22), 2674–2686."},"month":"11","publication_status":"published","type":"journal_article","author":[{"last_name":"Dolati","first_name":"Setareh","full_name":"Dolati, Setareh"},{"last_name":"Kage","first_name":"Frieda","full_name":"Kage, Frieda"},{"full_name":"Mueller, Jan","first_name":"Jan","last_name":"Mueller"},{"last_name":"Müsken","full_name":"Müsken, Mathias","first_name":"Mathias"},{"last_name":"Kirchner","full_name":"Kirchner, Marieluise","first_name":"Marieluise"},{"full_name":"Dittmar, Gunnar","first_name":"Gunnar","last_name":"Dittmar"},{"full_name":"Sixt, Michael K","first_name":"Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Klemens","full_name":"Rottner, Klemens","last_name":"Rottner"},{"full_name":"Falcke, Martin","first_name":"Martin","last_name":"Falcke"}],"file_date_updated":"2020-07-14T12:47:15Z","quality_controlled":"1","day":"01","fulldoi":"https://doi.org/10.1091/mbc.e18-02-0082","das_tickbox":"1","doi":"10.1091/mbc.e18-02-0082","year":"2018","volume":29,"abstract":[{"text":"Lamellipodia are flat membrane protrusions formed during mesenchymal motion. Polymerization at the leading edge assembles the actin filament network and generates protrusion force. How this force is supported by the network and how the assembly rate is shared between protrusion and network retrograde flow determines the protrusion rate. We use mathematical modeling to understand experiments changing the F-actin density in lamellipodia of B16-F1 melanoma cells by modulation of Arp2/3 complex activity or knockout of the formins FMNL2 and FMNL3. Cells respond to a reduction of density with a decrease of protrusion velocity, an increase in the ratio of force to filament number, but constant network assembly rate. The relation between protrusion force and tension gradient in the F-actin network and the density dependency of friction, elasticity, and viscosity of the network explain the experimental observations. The formins act as filament nucleators and elongators with differential rates. Modulation of their activity suggests an effect on network assembly rate. Contrary to these expectations, the effect of changes in elongator composition is much weaker than the consequences of the density change. We conclude that the force acting on the leading edge membrane is the force required to drive F-actin network retrograde flow.","lang":"eng"}],"publisher":"American Society for Cell Biology","external_id":{"pmid":["30156465"],"isi":["000455641000011"]},"page":"2674-2686","publication":"Molecular Biology of the Cell","pmid":1,"publication_identifier":{"eissn":["1939-4586"]},"department":[{"_id":"MiSi"}],"oa":1,"_id":"5992","intvolume":"        29","scopus_import":"1","title":"On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility","date_published":"2018-11-01T00:00:00Z"},{"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"citation":{"short":"S. Hross, F.J. Theis, M.K. Sixt, J. Hasenauer, Journal of the Royal Society Interface 15 (2018).","ista":"Hross S, Theis FJ, Sixt MK, Hasenauer J. 2018. Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data. Journal of the Royal Society Interface. 15(149), 20180600.","mla":"Hross, Sabrina, et al. “Mechanistic Description of Spatial Processes Using Integrative Modelling of Noise-Corrupted Imaging Data.” <i>Journal of the Royal Society Interface</i>, vol. 15, no. 149, 20180600, Royal Society, 2018, doi:<a href=\"https://doi.org/10.1098/rsif.2018.0600\">10.1098/rsif.2018.0600</a>.","chicago":"Hross, Sabrina, Fabian J. Theis, Michael K Sixt, and Jan Hasenauer. “Mechanistic Description of Spatial Processes Using Integrative Modelling of Noise-Corrupted Imaging Data.” <i>Journal of the Royal Society Interface</i>. Royal Society, 2018. <a href=\"https://doi.org/10.1098/rsif.2018.0600\">https://doi.org/10.1098/rsif.2018.0600</a>.","apa":"Hross, S., Theis, F. J., Sixt, M. K., &#38; Hasenauer, J. (2018). Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data. <i>Journal of the Royal Society Interface</i>. Royal Society. <a href=\"https://doi.org/10.1098/rsif.2018.0600\">https://doi.org/10.1098/rsif.2018.0600</a>","ieee":"S. Hross, F. J. Theis, M. K. Sixt, and J. Hasenauer, “Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data,” <i>Journal of the Royal Society Interface</i>, vol. 15, no. 149. Royal Society, 2018.","ama":"Hross S, Theis FJ, Sixt MK, Hasenauer J. Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data. <i>Journal of the Royal Society Interface</i>. 2018;15(149). doi:<a href=\"https://doi.org/10.1098/rsif.2018.0600\">10.1098/rsif.2018.0600</a>"},"oa_version":"Published Version","month":"12","publication_status":"published","type":"journal_article","author":[{"first_name":"Sabrina","full_name":"Hross, Sabrina","last_name":"Hross"},{"full_name":"Theis, Fabian J.","first_name":"Fabian J.","last_name":"Theis"},{"first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt"},{"last_name":"Hasenauer","first_name":"Jan","full_name":"Hasenauer, Jan"}],"file_date_updated":"2020-07-14T12:47:13Z","quality_controlled":"1","status":"public","has_accepted_license":"1","language":[{"iso":"eng"}],"ddc":["570"],"issue":"149","isi":1,"file":[{"file_size":1464288,"access_level":"open_access","file_id":"5925","content_type":"application/pdf","checksum":"56eb4308a15b7190bff938fab1f780e8","file_name":"2018_Interface_Hross.pdf","creator":"dernst","date_updated":"2020-07-14T12:47:13Z","date_created":"2019-02-05T14:46:44Z","relation":"main_file"}],"date_updated":"2026-08-12T06:28:50Z","date_created":"2019-01-20T22:59:18Z","publication_identifier":{"issn":["1742-5689"]},"oa":1,"department":[{"_id":"MiSi"}],"_id":"5858","article_number":"20180600","intvolume":"        15","scopus_import":"1","title":"Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data","date_published":"2018-12-05T00:00:00Z","day":"05","fulldoi":"https://doi.org/10.1098/rsif.2018.0600","year":"2018","doi":"10.1098/rsif.2018.0600","volume":15,"abstract":[{"text":"Spatial patterns are ubiquitous on the subcellular, cellular and tissue level, and can be studied using imaging techniques such as light and fluorescence microscopy. Imaging data provide quantitative information about biological systems; however, mechanisms causing spatial patterning often remain elusive. In recent years, spatio-temporal mathematical modelling has helped to overcome this problem. Yet, outliers and structured noise limit modelling of whole imaging data, and models often consider spatial summary statistics. Here, we introduce an integrated data-driven modelling approach that can cope with measurement artefacts and whole imaging data. Our approach combines mechanistic models of the biological processes with robust statistical models of the measurement process. The parameters of the integrated model are calibrated using a maximum-likelihood approach. We used this integrated modelling approach to study in vivo gradients of the chemokine (C-C motif) ligand 21 (CCL21). CCL21 gradients guide dendritic cells and are important in the adaptive immune response. Using artificial data, we verified that the integrated modelling approach provides reliable parameter estimates in the presence of measurement noise and that bias and variance of these estimates are reduced compared to conventional approaches. The application to experimental data allowed the parametrization and subsequent refinement of the model using additional mechanisms. Among other results, model-based hypothesis testing predicted lymphatic vessel-dependent concentration of heparan sulfate, the binding partner of CCL21. The selected model provided an accurate description of the experimental data and was partially validated using published data. Our findings demonstrate that integrated statistical modelling of whole imaging data is computationally feasible and can provide novel biological insights.","lang":"eng"}],"publisher":"Royal Society","external_id":{"isi":["000456783800011"]},"publication":"Journal of the Royal Society Interface"},{"date_published":"2018-05-18T00:00:00Z","intvolume":"        19","title":"Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells","scopus_import":"1","_id":"15","department":[{"_id":"MiSi"},{"_id":"Bio"}],"oa":1,"pmid":1,"publisher":"Nature Publishing Group","page":"606 - 616","publication":"Nature Immunology","external_id":{"isi":["000433041500026"],"pmid":["29777221"]},"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pubmed/29777221","open_access":"1"}],"ec_funded":1,"abstract":[{"lang":"eng","text":"Although much is known about the physiological framework of T cell motility, and numerous rate-limiting molecules have been identified through loss-of-function approaches, an integrated functional concept of T cell motility is lacking. Here, we used in vivo precision morphometry together with analysis of cytoskeletal dynamics in vitro to deconstruct the basic mechanisms of T cell migration within lymphatic organs. We show that the contributions of the integrin LFA-1 and the chemokine receptor CCR7 are complementary rather than positioned in a linear pathway, as they are during leukocyte extravasation from the blood vasculature. Our data demonstrate that CCR7 controls cortical actin flows, whereas integrins mediate substrate friction that is sufficient to drive locomotion in the absence of considerable surface adhesions and plasma membrane flux."}],"project":[{"_id":"25FE9508-B435-11E9-9278-68D0E5697425","name":"Cellular Navigation Along Spatial Gradients","grant_number":"724373","call_identifier":"H2020"},{"call_identifier":"H2020","grant_number":"747687","name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells","_id":"260AA4E2-B435-11E9-9278-68D0E5697425"},{"_id":"25A48D24-B435-11E9-9278-68D0E5697425","name":"Molecular and system level view of immune cell migration","grant_number":"ALTF 1396-2014"},{"name":"Cytoskeletal force generation and force transduction of migrating leukocytes","_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","grant_number":"281556"}],"volume":19,"year":"2018","doi":"10.1038/s41590-018-0109-z","day":"18","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).","fulldoi":"https://doi.org/10.1038/s41590-018-0109-z","quality_controlled":"1","type":"journal_article","author":[{"first_name":"Miroslav","full_name":"Hons, Miroslav","id":"4167FE56-F248-11E8-B48F-1D18A9856A87","last_name":"Hons","orcid":"0000-0002-6625-3348"},{"last_name":"Kopf","id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-2187-6656","full_name":"Kopf, Aglaja","first_name":"Aglaja"},{"last_name":"Hauschild","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9843-3522","full_name":"Hauschild, Robert","first_name":"Robert"},{"first_name":"Alexander F","full_name":"Leithner, Alexander F","orcid":"0000-0002-1073-744X","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","last_name":"Leithner"},{"full_name":"Gärtner, Florian R","first_name":"Florian R","last_name":"Gärtner","id":"397A88EE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6120-3723"},{"full_name":"Abe, Jun","first_name":"Jun","last_name":"Abe"},{"orcid":"0000-0003-2856-3369","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","last_name":"Renkawitz","first_name":"Jörg","full_name":"Renkawitz, Jörg"},{"first_name":"Jens","full_name":"Stein, Jens","last_name":"Stein"},{"orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","first_name":"Michael K","full_name":"Sixt, Michael K"}],"publication_status":"published","month":"05","oa_version":"Published Version","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.","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.","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>","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>","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.","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>."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","date_created":"2018-12-11T11:44:10Z","date_updated":"2026-11-14T23:30:20Z","issue":"6","isi":1,"language":[{"iso":"eng"}],"related_material":{"record":[{"relation":"dissertation_contains","id":"6891","status":"public"}]},"ddc":["570"],"publist_id":"8040","status":"public","acknowledged_ssus":[{"_id":"SSU"}]},{"month":"04","oa_version":"Published Version","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"citation":{"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>.","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>","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>","ieee":"A. F. Leithner, “Branched actin networks in dendritic cell biology,” Institute of Science and Technology Austria, 2018.","ista":"Leithner AF. 2018. Branched actin networks in dendritic cell biology. Institute of Science and Technology Austria.","short":"A.F. Leithner, Branched Actin Networks in Dendritic Cell Biology, Institute of Science and Technology Austria, 2018.","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>."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","article_processing_charge":"No","file_date_updated":"2021-02-11T23:30:17Z","type":"dissertation","author":[{"orcid":"0000-0002-1073-744X","last_name":"Leithner","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","full_name":"Leithner, Alexander F","first_name":"Alexander F"}],"supervisor":[{"full_name":"Sixt, Michael K","first_name":"Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"alternative_title":["ISTA Thesis"],"publication_status":"published","degree_awarded":"PhD","related_material":{"record":[{"status":"public","relation":"part_of_dissertation","id":"1321"}]},"language":[{"iso":"eng"}],"ddc":["571","599","610"],"publist_id":"7542","status":"public","has_accepted_license":"1","acknowledged_ssus":[{"_id":"NanoFab"},{"_id":"Bio"},{"_id":"PreCl"},{"_id":"EM-Fac"}],"date_updated":"2025-09-22T08:27:34Z","pubrep_id":"998","date_created":"2018-12-11T11:45:49Z","file":[{"file_id":"6219","file_size":29027671,"embargo_to":"open_access","access_level":"closed","date_created":"2019-04-05T09:23:11Z","date_updated":"2021-02-11T23:30:17Z","relation":"source_file","file_name":"PhD_thesis_AlexLeithner_final_version.docx","creator":"dernst","checksum":"d5e3edbac548c26c1fa43a4b37a54a4c","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document"},{"creator":"dernst","file_name":"PhD_thesis_AlexLeithner.pdf","date_created":"2019-04-05T09:23:11Z","date_updated":"2021-02-11T11:17:16Z","relation":"main_file","embargo":"2019-04-15","content_type":"application/pdf","checksum":"071f7476db29e41146824ebd0697cb10","file_id":"6220","access_level":"open_access","file_size":66045341}],"_id":"323","department":[{"_id":"MiSi"}],"oa":1,"publication_identifier":{"issn":["2663-337X"]},"corr_author":"1","date_published":"2018-04-12T00:00:00Z","title":"Branched actin networks in dendritic cell biology","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"}],"year":"2018","doi":"10.15479/AT:ISTA:th_998","day":"12","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.","fulldoi":"https://doi.org/10.15479/AT:ISTA:th_998","publisher":"Institute of Science and Technology Austria","page":"99"},{"quality_controlled":"1","author":[{"first_name":"Markus","full_name":"Brown, Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","last_name":"Brown"},{"orcid":"0000-0003-3470-6119","last_name":"Assen","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","full_name":"Assen, Frank P","first_name":"Frank P"},{"first_name":"Alexander F","full_name":"Leithner, Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","last_name":"Leithner","orcid":"0000-0002-1073-744X"},{"full_name":"Abe, Jun","first_name":"Jun","last_name":"Abe"},{"last_name":"Schachner","full_name":"Schachner, Helga","first_name":"Helga"},{"last_name":"Asfour","full_name":"Asfour, Gabriele","first_name":"Gabriele"},{"full_name":"Bagó Horváth, Zsuzsanna","first_name":"Zsuzsanna","last_name":"Bagó Horváth"},{"last_name":"Stein","full_name":"Stein, Jens","first_name":"Jens"},{"first_name":"Pavel","full_name":"Uhrin, Pavel","last_name":"Uhrin"},{"full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"},{"last_name":"Kerjaschki","full_name":"Kerjaschki, Dontscho","first_name":"Dontscho"}],"type":"journal_article","publication_status":"published","month":"03","oa_version":"Published Version","citation":{"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>.","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.","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>","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.","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.","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_processing_charge":"No","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_created":"2018-12-11T11:46:16Z","date_updated":"2026-11-14T23:30:45Z","issue":"6382","isi":1,"language":[{"iso":"eng"}],"ddc":["570"],"related_material":{"record":[{"id":"6947","relation":"dissertation_contains","status":"public"}]},"publist_id":"7428","status":"public","acknowledged_ssus":[{"_id":"Bio"}],"date_published":"2018-03-23T00:00:00Z","article_type":"original","title":"Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice","scopus_import":"1","intvolume":"       359","_id":"402","department":[{"_id":"MiSi"}],"oa":1,"corr_author":"1","pmid":1,"publication":"Science","page":"1408 - 1411","external_id":{"pmid":["29567714"],"isi":["000428043600047"]},"publisher":"American Association for the Advancement of Science","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1126/science.aal3662"}],"abstract":[{"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.","lang":"eng"}],"ec_funded":1,"volume":359,"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"},{"_id":"25A603A2-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes","grant_number":"281556","call_identifier":"FP7"}],"year":"2018","doi":"10.1126/science.aal3662","fulldoi":"https://doi.org/10.1126/science.aal3662","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.","day":"23"},{"intvolume":"        27","title":"Cell migration: Making the waves","scopus_import":"1","article_type":"letter_note","date_published":"2017-01-09T00:00:00Z","oa":1,"department":[{"_id":"MiSi"}],"publication_identifier":{"issn":["09609822"]},"_id":"1161","main_file_link":[{"url":"https://doi.org/10.1016/j.cub.2016.11.035","open_access":"1"}],"publisher":"Cell Press","page":"R24 - R25","publication":"Current Biology","external_id":{"isi":["000391902500010"]},"doi":"10.1016/j.cub.2016.11.035","year":"2017","OA_type":"free access","day":"09","fulldoi":"https://doi.org/10.1016/j.cub.2016.11.035","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"}],"volume":27,"type":"journal_article","author":[{"full_name":"Müller, Jan","first_name":"Jan","last_name":"Müller","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D"},{"orcid":"0000-0002-6620-9179","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","first_name":"Michael K"}],"publication_status":"published","quality_controlled":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","month":"01","oa_version":"Published Version","citation":{"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>.","short":"J. Müller, M.K. Sixt, Current Biology 27 (2017) R24–R25.","ista":"Müller J, Sixt MK. 2017. Cell migration: Making the waves. Current Biology. 27(1), R24–R25.","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>","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.","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>","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>."},"date_created":"2018-12-11T11:50:29Z","date_updated":"2026-06-18T17:20:13Z","status":"public","publist_id":"6197","issue":"1","isi":1,"language":[{"iso":"eng"}],"OA_place":"publisher","ddc":["570"]},{"keyword":["Immunological synapse"],"fulldoi":"https://doi.org/10.15479/AT:ISTA:71","day":"09","doi":"10.15479/AT:ISTA:71","has_accepted_license":"1","year":"2017","status":"public","ddc":["570"],"abstract":[{"lang":"eng","text":"Immunological synapse DC-Tcells"}],"file":[{"file_id":"5612","file_size":236204020,"access_level":"open_access","creator":"system","file_name":"IST-2017-71-v1+1_Synapse_1.avi","date_updated":"2020-07-14T12:47:04Z","date_created":"2018-12-12T13:02:47Z","relation":"main_file","content_type":"video/x-msvideo","checksum":"3d6942d47d0737d064706b5728c4d8c8"},{"checksum":"4850006c047b0147a9e85b3c2f6f0af4","content_type":"video/x-msvideo","relation":"main_file","date_created":"2018-12-12T13:02:51Z","date_updated":"2020-07-14T12:47:04Z","file_name":"IST-2017-71-v1+2_Synapse_2.avi","creator":"system","file_size":226232496,"access_level":"open_access","file_id":"5613"}],"date_updated":"2024-02-21T13:47:00Z","date_created":"2018-12-12T12:31:34Z","publisher":"Institute of Science and Technology Austria","article_processing_charge":"No","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","oa":1,"department":[{"_id":"MiSi"}],"datarep_id":"71","tmp":{"name":"Creative Commons Public Domain Dedication (CC0 1.0)","legal_code_url":"https://creativecommons.org/publicdomain/zero/1.0/legalcode","short":"CC0 (1.0)","image":"/images/cc_0.png"},"citation":{"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>","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>","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>.","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>.","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>.","short":"A.F. Leithner, (2017)."},"oa_version":"Published Version","_id":"5567","month":"08","author":[{"id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","last_name":"Leithner","orcid":"0000-0002-1073-744X","first_name":"Alexander F","full_name":"Leithner, Alexander F"}],"title":"Immunological synapse DC-Tcells","type":"research_data","date_published":"2017-08-09T00:00:00Z","file_date_updated":"2020-07-14T12:47:04Z"},{"date_published":"2017-11-06T00:00:00Z","scopus_import":"1","title":"Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments","intvolume":"         6","article_number":"e30867","_id":"569","publication_identifier":{"issn":["2050-084X"]},"oa":1,"department":[{"_id":"MiSi"}],"external_id":{"isi":["000414407700001"]},"publication":"eLife","publisher":"eLife Sciences Publications","volume":6,"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"}],"fulldoi":"https://doi.org/10.7554/eLife.30867","day":"06","year":"2017","doi":"10.7554/eLife.30867","file_date_updated":"2020-07-14T12:47:10Z","quality_controlled":"1","publication_status":"published","author":[{"last_name":"Spira","full_name":"Spira, Felix","first_name":"Felix"},{"last_name":"Cuylen Haering","first_name":"Sara","full_name":"Cuylen Haering, Sara"},{"last_name":"Mehta","full_name":"Mehta, Shalin","first_name":"Shalin"},{"full_name":"Samwer, Matthias","first_name":"Matthias","last_name":"Samwer"},{"full_name":"Reversat, Anne","first_name":"Anne","orcid":"0000-0003-0666-8928","last_name":"Reversat","id":"35B76592-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Verma","full_name":"Verma, Amitabh","first_name":"Amitabh"},{"last_name":"Oldenbourg","full_name":"Oldenbourg, Rudolf","first_name":"Rudolf"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","orcid":"0000-0002-6620-9179","first_name":"Michael K","full_name":"Sixt, Michael K"},{"last_name":"Gerlich","first_name":"Daniel","full_name":"Gerlich, Daniel"}],"type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"citation":{"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>.","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>","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.","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>","short":"F. Spira, S. Cuylen Haering, S. Mehta, M. Samwer, A. Reversat, A. Verma, R. Oldenbourg, M.K. Sixt, D. Gerlich, ELife 6 (2017).","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.","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>."},"oa_version":"Published Version","month":"11","article_processing_charge":"No","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","date_updated":"2025-09-11T07:41:10Z","pubrep_id":"919","date_created":"2018-12-11T11:47:14Z","file":[{"checksum":"ba09c1451153d39e4f4b7cee013e314c","content_type":"application/pdf","relation":"main_file","date_updated":"2020-07-14T12:47:10Z","date_created":"2018-12-12T10:10:40Z","creator":"system","file_name":"IST-2017-919-v1+1_elife-30867-figures-v1.pdf","file_size":9666973,"access_level":"open_access","file_id":"4829"},{"checksum":"01eb51f1d6ad679947415a51c988e137","content_type":"application/pdf","date_created":"2018-12-12T10:10:41Z","relation":"main_file","date_updated":"2020-07-14T12:47:10Z","file_name":"IST-2017-919-v1+2_elife-30867-v1.pdf","creator":"system","access_level":"open_access","file_size":5951246,"file_id":"4830"}],"ddc":["570"],"language":[{"iso":"eng"}],"isi":1,"has_accepted_license":"1","publist_id":"7245","status":"public"},{"language":[{"iso":"eng"}],"issue":"6","isi":1,"status":"public","publist_id":"7243","date_updated":"2025-09-11T07:39:45Z","date_created":"2018-12-11T11:47:15Z","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>.","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.","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 <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.","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>","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>","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>."},"oa_version":"None","month":"11","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","article_processing_charge":"No","quality_controlled":"1","publication_status":"published","type":"journal_article","author":[{"full_name":"Gärtner, Florian R","first_name":"Florian R","orcid":"0000-0001-6120-3723","last_name":"Gärtner","id":"397A88EE-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Ahmad","first_name":"Zerkah","full_name":"Ahmad, Zerkah"},{"first_name":"Gerhild","full_name":"Rosenberger, Gerhild","last_name":"Rosenberger"},{"full_name":"Fan, Shuxia","first_name":"Shuxia","last_name":"Fan"},{"first_name":"Leo","full_name":"Nicolai, Leo","last_name":"Nicolai"},{"last_name":"Busch","first_name":"Benjamin","full_name":"Busch, Benjamin"},{"first_name":"Gökce","full_name":"Yavuz, Gökce","last_name":"Yavuz"},{"last_name":"Luckner","full_name":"Luckner, Manja","first_name":"Manja"},{"first_name":"Hellen","full_name":"Ishikawa Ankerhold, Hellen","last_name":"Ishikawa Ankerhold"},{"first_name":"Roman","full_name":"Hennel, Roman","last_name":"Hennel"},{"last_name":"Benechet","full_name":"Benechet, Alexandre","first_name":"Alexandre"},{"last_name":"Lorenz","first_name":"Michael","full_name":"Lorenz, Michael"},{"first_name":"Sue","full_name":"Chandraratne, Sue","last_name":"Chandraratne"},{"last_name":"Schubert","first_name":"Irene","full_name":"Schubert, Irene"},{"full_name":"Helmer, Sebastian","first_name":"Sebastian","last_name":"Helmer"},{"first_name":"Bianca","full_name":"Striednig, Bianca","last_name":"Striednig"},{"last_name":"Stark","full_name":"Stark, Konstantin","first_name":"Konstantin"},{"last_name":"Janko","full_name":"Janko, Marek","first_name":"Marek"},{"full_name":"Böttcher, Ralph","first_name":"Ralph","last_name":"Böttcher"},{"first_name":"Admar","full_name":"Verschoor, Admar","last_name":"Verschoor"},{"last_name":"Leon","full_name":"Leon, Catherine","first_name":"Catherine"},{"first_name":"Christian","full_name":"Gachet, Christian","last_name":"Gachet"},{"last_name":"Gudermann","first_name":"Thomas","full_name":"Gudermann, Thomas"},{"last_name":"Mederos Y Schnitzler","first_name":"Michael","full_name":"Mederos Y Schnitzler, Michael"},{"first_name":"Zachary","full_name":"Pincus, Zachary","last_name":"Pincus"},{"first_name":"Matteo","full_name":"Iannacone, Matteo","last_name":"Iannacone"},{"last_name":"Haas","first_name":"Rainer","full_name":"Haas, Rainer"},{"last_name":"Wanner","first_name":"Gerhard","full_name":"Wanner, Gerhard"},{"last_name":"Lauber","first_name":"Kirsten","full_name":"Lauber, Kirsten"},{"orcid":"0000-0002-6620-9179","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","first_name":"Michael K"},{"full_name":"Massberg, Steffen","first_name":"Steffen","last_name":"Massberg"}],"project":[{"grant_number":"747687","call_identifier":"H2020","_id":"260AA4E2-B435-11E9-9278-68D0E5697425","name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells"}],"volume":171,"ec_funded":1,"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."}],"day":"30","fulldoi":"https://doi.org/10.1016/j.cell.2017.11.001","year":"2017","doi":"10.1016/j.cell.2017.11.001","publisher":"Cell Press","publication":"Cell Press","page":"1368 - 1382","external_id":{"isi":["000417362700018"]},"_id":"571","publication_identifier":{"issn":["0092-8674"]},"department":[{"_id":"MiSi"}],"date_published":"2017-11-30T00:00:00Z","intvolume":"       171","scopus_import":"1","title":"Migrating platelets are mechano scavengers that collect and bundle bacteria"},{"date_created":"2018-12-11T11:47:46Z","pubrep_id":"902","date_updated":"2025-09-11T07:09:28Z","file":[{"file_size":9523746,"access_level":"open_access","file_id":"5072","checksum":"dae30190291c3630e8102d8714a8d23e","content_type":"application/pdf","relation":"main_file","date_created":"2018-12-12T10:14:21Z","date_updated":"2020-07-14T12:47:34Z","creator":"system","file_name":"IST-2017-902-v1+1_Kage_et_al-2017-Nature_Communications.pdf"}],"isi":1,"ddc":["570"],"language":[{"iso":"eng"}],"publist_id":"7075","status":"public","has_accepted_license":"1","quality_controlled":"1","file_date_updated":"2020-07-14T12:47:34Z","type":"journal_article","author":[{"last_name":"Kage","full_name":"Kage, Frieda","first_name":"Frieda"},{"last_name":"Winterhoff","first_name":"Moritz","full_name":"Winterhoff, Moritz"},{"last_name":"Dimchev","full_name":"Dimchev, Vanessa","first_name":"Vanessa"},{"id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D","last_name":"Müller","first_name":"Jan","full_name":"Müller, Jan"},{"last_name":"Thalheim","first_name":"Tobias","full_name":"Thalheim, 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"},{"full_name":"Block, Jennifer","first_name":"Jennifer","last_name":"Block"},{"first_name":"Georgi A","full_name":"Dimchev, Georgi A","last_name":"Dimchev"},{"last_name":"Geyer","full_name":"Geyer, Matthias","first_name":"Matthias"},{"first_name":"Hams","full_name":"Schnittler, Hams","last_name":"Schnittler"},{"first_name":"Cord","full_name":"Brakebusch, Cord","last_name":"Brakebusch"},{"last_name":"Stradal","first_name":"Theresia","full_name":"Stradal, Theresia"},{"first_name":"Marie","full_name":"Carlier, Marie","last_name":"Carlier"},{"first_name":"Michael K","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","orcid":"0000-0002-6620-9179"},{"first_name":"Josef","full_name":"Käs, Josef","last_name":"Käs"},{"first_name":"Jan","full_name":"Faix, Jan","last_name":"Faix"},{"last_name":"Rottner","first_name":"Klemens","full_name":"Rottner, Klemens"}],"publication_status":"published","month":"03","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"oa_version":"Published Version","citation":{"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>","ieee":"F. Kage <i>et al.</i>, “FMNL formins boost lamellipodial force generation,” <i>Nature Communications</i>, vol. 8. Nature Publishing Group, 2017.","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>","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>.","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>.","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.","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":"317138e5-6ab7-11ef-aa6d-ffef3953e345","article_processing_charge":"No","publisher":"Nature Publishing Group","external_id":{"isi":["000396993700001"]},"publication":"Nature Communications","abstract":[{"lang":"eng","text":"Migration frequently involves Rac-mediated protrusion of lamellipodia, formed by Arp2/3 complex-dependent branching thought to be crucial for force generation and stability of these networks. The formins FMNL2 and FMNL3 are Cdc42 effectors targeting to the lamellipodium tip and shown here to nucleate and elongate actin filaments with complementary activities in vitro. In migrating B16-F1 melanoma cells, both formins contribute to the velocity of lamellipodium protrusion. Loss of FMNL2/3 function in melanoma cells and fibroblasts reduces lamellipodial width, actin filament density and -bundling, without changing patterns of Arp2/3 complex incorporation. Strikingly, in melanoma cells, FMNL2/3 gene inactivation almost completely abolishes protrusion forces exerted by lamellipodia and modifies their ultrastructural organization. Consistently, CRISPR/Cas-mediated depletion of FMNL2/3 in fibroblasts reduces both migration and capability of cells to move against viscous media. Together, we conclude that force generation in lamellipodia strongly depends on FMNL formin activity, operating in addition to Arp2/3 complex-dependent filament branching."}],"volume":8,"year":"2017","doi":"10.1038/ncomms14832","day":"22","fulldoi":"https://doi.org/10.1038/ncomms14832","date_published":"2017-03-22T00:00:00Z","intvolume":"         8","article_number":"14832","title":"FMNL formins boost lamellipodial force generation","scopus_import":"1","_id":"659","oa":1,"department":[{"_id":"MiSi"}],"publication_identifier":{"issn":["2041-1723"]}},{"_id":"668","department":[{"_id":"MiSi"}],"oa":1,"publication_identifier":{"issn":["0021-9258"]},"date_published":"2017-04-28T00:00:00Z","article_type":"original","scopus_import":"1","title":"Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion","intvolume":"       292","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"}],"volume":292,"year":"2017","doi":"10.1074/jbc.M116.766923","fulldoi":"https://doi.org/10.1074/jbc.M116.766923","day":"28","external_id":{"isi":["000400478300035"]},"publication":"Journal of Biological Chemistry","page":"7258 - 7273","publisher":"American Society for Biochemistry and Molecular Biology","month":"04","oa_version":"Published Version","citation":{"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>.","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.","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>","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>","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.","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.” <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>."},"article_processing_charge":"No","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","quality_controlled":"1","file_date_updated":"2020-07-14T12:47:37Z","author":[{"full_name":"Horsthemke, Markus","first_name":"Markus","last_name":"Horsthemke"},{"last_name":"Bachg","first_name":"Anne","full_name":"Bachg, Anne"},{"last_name":"Groll","first_name":"Katharina","full_name":"Groll, Katharina"},{"full_name":"Moyzio, Sven","first_name":"Sven","last_name":"Moyzio"},{"last_name":"Müther","full_name":"Müther, Barbara","first_name":"Barbara"},{"last_name":"Hemkemeyer","full_name":"Hemkemeyer, Sandra","first_name":"Sandra"},{"first_name":"Roland","full_name":"Wedlich Söldner, Roland","last_name":"Wedlich Söldner"},{"first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt"},{"first_name":"Sebastian","full_name":"Tacke, Sebastian","last_name":"Tacke"},{"last_name":"Bähler","first_name":"Martin","full_name":"Bähler, Martin"},{"last_name":"Hanley","full_name":"Hanley, Peter","first_name":"Peter"}],"type":"journal_article","publication_status":"published","isi":1,"issue":"17","language":[{"iso":"eng"}],"ddc":["570"],"has_accepted_license":"1","status":"public","publist_id":"7059","date_updated":"2025-09-11T07:03:17Z","date_created":"2018-12-11T11:47:49Z","file":[{"relation":"main_file","date_created":"2019-10-24T15:25:42Z","date_updated":"2020-07-14T12:47:37Z","file_name":"2017_JBC_Horsthemke.pdf","creator":"dernst","checksum":"d488162874326a4bb056065fa549dc4a","content_type":"application/pdf","file_id":"6971","file_size":5647880,"access_level":"open_access"}]},{"date_created":"2018-12-11T11:47:50Z","date_updated":"2025-09-10T14:27:34Z","pubrep_id":"900","file":[{"file_name":"IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf","creator":"system","date_updated":"2020-07-14T12:47:38Z","date_created":"2018-12-12T10:14:54Z","relation":"main_file","content_type":"application/pdf","checksum":"8fdddaab1f1d76a6ec9ca94dcb6b07a2","file_id":"5109","file_size":2248814,"access_level":"open_access"}],"isi":1,"issue":"5","ddc":["570"],"language":[{"iso":"eng"}],"has_accepted_license":"1","status":"public","publist_id":"7052","quality_controlled":"1","file_date_updated":"2020-07-14T12:47:38Z","author":[{"orcid":"0000-0001-7829-3518","last_name":"Vaahtomeri","id":"368EE576-F248-11E8-B48F-1D18A9856A87","full_name":"Vaahtomeri, Kari","first_name":"Kari"},{"id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","last_name":"Brown","first_name":"Markus","full_name":"Brown, Markus"},{"last_name":"Hauschild","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9843-3522","full_name":"Hauschild, Robert","first_name":"Robert"},{"full_name":"De Vries, Ingrid","first_name":"Ingrid","last_name":"De Vries","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Leithner, Alexander F","first_name":"Alexander F","orcid":"0000-0002-1073-744X","last_name":"Leithner","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87"},{"id":"3C23B994-F248-11E8-B48F-1D18A9856A87","last_name":"Mehling","orcid":"0000-0001-8599-1226","first_name":"Matthias","full_name":"Mehling, Matthias"},{"full_name":"Kaufmann, Walter","first_name":"Walter","last_name":"Kaufmann","id":"3F99E422-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9735-5315"},{"last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K"}],"type":"journal_article","publication_status":"published","month":"05","oa_version":"Published Version","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":{"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.","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.","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.” <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>."},"article_processing_charge":"Yes","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","page":"902 - 909","external_id":{"isi":["000402124100002"]},"publication":"Cell Reports","publisher":"Cell Press","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,"volume":19,"project":[{"call_identifier":"FP7","grant_number":"281556","name":"Cytoskeletal force generation and force transduction of migrating leukocytes","_id":"25A603A2-B435-11E9-9278-68D0E5697425"},{"grant_number":"Y 564-B12","call_identifier":"FWF","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes"}],"doi":"10.1016/j.celrep.2017.04.027","year":"2017","fulldoi":"https://doi.org/10.1016/j.celrep.2017.04.027","day":"02","date_published":"2017-05-02T00:00:00Z","scopus_import":"1","title":"Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia","intvolume":"        19","_id":"672","oa":1,"department":[{"_id":"MiSi"},{"_id":"Bio"},{"_id":"EM-Fac"}],"corr_author":"1","publication_identifier":{"issn":["2211-1247"]}},{"_id":"674","department":[{"_id":"MiSi"},{"_id":"Bio"},{"_id":"NanoFab"}],"corr_author":"1","publication_identifier":{"issn":["09609822"]},"date_published":"2017-05-09T00:00:00Z","title":"Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6","scopus_import":"1","intvolume":"        27","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."}],"ec_funded":1,"volume":27,"project":[{"name":"International IST Postdoc Fellowship Programme","_id":"25681D80-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","grant_number":"291734"},{"grant_number":"Y 564-B12","call_identifier":"FWF","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes"}],"doi":"10.1016/j.cub.2017.04.004","year":"2017","fulldoi":"https://doi.org/10.1016/j.cub.2017.04.004","day":"09","page":"1314 - 1325","external_id":{"isi":["000400741700021"]},"publication":"Current Biology","publisher":"Cell Press","month":"05","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>.","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.","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>","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>."},"oa_version":"None","article_processing_charge":"No","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","quality_controlled":"1","author":[{"id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","last_name":"Schwarz","first_name":"Jan","full_name":"Schwarz, Jan"},{"full_name":"Bierbaum, Veronika","first_name":"Veronika","last_name":"Bierbaum","id":"3FD04378-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Kari","full_name":"Vaahtomeri, Kari","orcid":"0000-0001-7829-3518","id":"368EE576-F248-11E8-B48F-1D18A9856A87","last_name":"Vaahtomeri"},{"full_name":"Hauschild, Robert","first_name":"Robert","last_name":"Hauschild","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9843-3522"},{"full_name":"Brown, Markus","first_name":"Markus","last_name":"Brown","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Ingrid","full_name":"De Vries, Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","last_name":"De Vries"},{"orcid":"0000-0002-1073-744X","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","last_name":"Leithner","first_name":"Alexander F","full_name":"Leithner, Alexander F"},{"last_name":"Reversat","id":"35B76592-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-0666-8928","full_name":"Reversat, Anne","first_name":"Anne"},{"id":"4515C308-F248-11E8-B48F-1D18A9856A87","last_name":"Merrin","orcid":"0000-0001-5145-4609","first_name":"Jack","full_name":"Merrin, Jack"},{"last_name":"Tarrant","first_name":"Teresa","full_name":"Tarrant, Teresa"},{"orcid":"0000-0003-4398-476X","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","last_name":"Bollenbach","first_name":"Tobias","full_name":"Bollenbach, Tobias"},{"full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"}],"type":"journal_article","publication_status":"published","isi":1,"issue":"9","language":[{"iso":"eng"}],"publist_id":"7050","status":"public","date_updated":"2025-09-10T14:26:47Z","date_created":"2018-12-11T11:47:51Z"},{"fulldoi":"https://doi.org/10.1016/j.celrep.2017.04.051","day":"16","year":"2017","doi":"10.1016/j.celrep.2017.04.051","volume":19,"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."}],"external_id":{"isi":["000402125100002"]},"publication":"Cell Reports","page":"1294 - 1303","publisher":"Cell Press","publication_identifier":{"issn":["2211-1247"]},"oa":1,"department":[{"_id":"MiSi"}],"_id":"677","scopus_import":"1","title":"The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination","intvolume":"        19","date_published":"2017-05-16T00:00:00Z","has_accepted_license":"1","status":"public","publist_id":"7046","ddc":["570"],"language":[{"iso":"eng"}],"isi":1,"issue":"7","file":[{"file_size":3005610,"access_level":"open_access","file_id":"5171","content_type":"application/pdf","checksum":"efc7287d9c6354983cb151880e9ad72a","file_name":"IST-2017-899-v1+1_1-s2.0-S2211124717305454-main.pdf","creator":"system","date_created":"2018-12-12T10:15:48Z","date_updated":"2020-07-14T12:47:40Z","relation":"main_file"}],"date_updated":"2025-09-10T14:23:55Z","date_created":"2018-12-11T11:47:52Z","pubrep_id":"899","article_processing_charge":"No","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","citation":{"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>.","short":"C. Lademann, J. Renkawitz, B. Pfander, S. Jentsch, Cell Reports 19 (2017) 1294–1303.","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.","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>","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>","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>."},"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"},"oa_version":"Published Version","month":"05","publication_status":"published","author":[{"first_name":"Claudio","full_name":"Lademann, Claudio","last_name":"Lademann"},{"last_name":"Renkawitz","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2856-3369","full_name":"Renkawitz, Jörg","first_name":"Jörg"},{"last_name":"Pfander","full_name":"Pfander, Boris","first_name":"Boris"},{"last_name":"Jentsch","full_name":"Jentsch, Stefan","first_name":"Stefan"}],"type":"journal_article","file_date_updated":"2020-07-14T12:47:40Z","quality_controlled":"1"},{"issue":"13","isi":1,"ddc":["570"],"language":[{"iso":"eng"}],"has_accepted_license":"1","publist_id":"7008","status":"public","date_updated":"2025-09-10T11:13:35Z","date_created":"2018-12-11T11:47:58Z","file":[{"content_type":"application/pdf","checksum":"42c81a0a4fc3128883b391c3af3f74bc","file_name":"2017_CellScience_Vess.pdf","creator":"dernst","date_created":"2019-10-24T09:43:56Z","relation":"main_file","date_updated":"2020-07-14T12:47:45Z","access_level":"open_access","file_size":10847596,"file_id":"6966"}],"month":"07","citation":{"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>","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.","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.","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>."},"oa_version":"Published Version","article_processing_charge":"No","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","quality_controlled":"1","file_date_updated":"2020-07-14T12:47:45Z","author":[{"full_name":"Veß, Astrid","first_name":"Astrid","last_name":"Veß"},{"full_name":"Blache, Ulrich","first_name":"Ulrich","last_name":"Blache"},{"last_name":"Leitner","first_name":"Laura","full_name":"Leitner, Laura"},{"last_name":"Kurz","full_name":"Kurz, Angela","first_name":"Angela"},{"last_name":"Ehrenpfordt","first_name":"Anja","full_name":"Ehrenpfordt, Anja"},{"last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K"},{"first_name":"Guido","full_name":"Posern, Guido","last_name":"Posern"}],"type":"journal_article","publication_status":"published","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"}],"volume":130,"year":"2017","doi":"10.1242/jcs.200899","fulldoi":"https://doi.org/10.1242/jcs.200899","day":"01","pmid":1,"external_id":{"pmid":["28515231"],"isi":["000405612200009"]},"page":"2172 - 2184","publication":"Journal of Cell Science","publisher":"Company of Biologists","_id":"694","oa":1,"department":[{"_id":"MiSi"}],"publication_identifier":{"issn":["0021-9533"]},"date_published":"2017-07-01T00:00:00Z","article_type":"original","scopus_import":"1","title":"A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity","intvolume":"       130"}]