[{"volume":17,"acknowledgement":"Y. Fukui (Medical Institute of Bioregulation, Kyushu University) and J. Stein (Theodor Kocher Institute, University of Bern) are acknowledged for providing the DOCK8 deficient bone marrow. and H. Häcker (St. Judes Children's Research Hospital) for providing the ERHBD-HoxB8-encoding retroviral construct. pSpCas9(BB)-2a-Puro (PX459) was a gift from F. Zhang (Massachusetts Institute of Technology) (Addgene plasmid # 48139) and pGRG36 was a gift from N. Craig (Johns Hopkins University School of Medicine) (Addgene plasmid # 16666). LifeAct-GFP-encoding retrovirus was kindly provided by A. Leithner (Institute of Science and Technology Austria). pSIM8 and TKC E. coli were gifts from D.L. Court (Center for Cancer Research, National Cancer Institute). We acknowledge M. Gröger and S. Rauscher for excellent technical support (Core imaging facility, Medical University of Vienna). We thank D.P. Barlow and L.R. Cheever for critical reading of the manuscript. This work was supported by the Austrian Academy of Sciences, the Science Fund of the Austrian National Bank (14107) and the Austrian Science Fund FWF (I1620-B22) in the Infect-ERA framework (to S.Knapp).","citation":{"ista":"Martins R, Maier J, Gorki A, Huber K, Sharif O, Starkl P, Saluzzo S, Quattrone F, Gawish R, Lakovits K, Aichinger M, Radic Sarikas B, Lardeau C, Hladik A, Korosec A, Brown M, Vaahtomeri K, Duggan M, Kerjaschki D, Esterbauer H, Colinge J, Eisenbarth S, Decker T, Bennett K, Kubicek S, Sixt MK, Superti Furga G, Knapp S. 2016. Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nature Immunology. 17(12), 1361–1372.","short":"R. Martins, J. Maier, A. Gorki, K. Huber, O. Sharif, P. Starkl, S. Saluzzo, F. Quattrone, R. Gawish, K. Lakovits, M. Aichinger, B. Radic Sarikas, C. Lardeau, A. Hladik, A. Korosec, M. Brown, K. Vaahtomeri, M. Duggan, D. Kerjaschki, H. Esterbauer, J. Colinge, S. Eisenbarth, T. Decker, K. Bennett, S. Kubicek, M.K. Sixt, G. Superti Furga, S. Knapp, Nature Immunology 17 (2016) 1361–1372.","mla":"Martins, Rui, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection via Disruption of Phagocyte Functions.” <i>Nature Immunology</i>, vol. 17, no. 12, Nature Publishing Group, 2016, pp. 1361–72, doi:<a href=\"https://doi.org/10.1038/ni.3590\">10.1038/ni.3590</a>.","ieee":"R. Martins <i>et al.</i>, “Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions,” <i>Nature Immunology</i>, vol. 17, no. 12. Nature Publishing Group, pp. 1361–1372, 2016.","chicago":"Martins, Rui, Julia Maier, Anna Gorki, Kilian Huber, Omar Sharif, Philipp Starkl, Simona Saluzzo, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection via Disruption of Phagocyte Functions.” <i>Nature Immunology</i>. Nature Publishing Group, 2016. <a href=\"https://doi.org/10.1038/ni.3590\">https://doi.org/10.1038/ni.3590</a>.","ama":"Martins R, Maier J, Gorki A, et al. Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. <i>Nature Immunology</i>. 2016;17(12):1361-1372. doi:<a href=\"https://doi.org/10.1038/ni.3590\">10.1038/ni.3590</a>","apa":"Martins, R., Maier, J., Gorki, A., Huber, K., Sharif, O., Starkl, P., … Knapp, S. (2016). Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. <i>Nature Immunology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/ni.3590\">https://doi.org/10.1038/ni.3590</a>"},"year":"2016","date_updated":"2021-01-12T06:48:36Z","abstract":[{"text":"Hemolysis drives susceptibility to bacterial infections and predicts poor outcome from sepsis. These detrimental effects are commonly considered to be a consequence of heme-iron serving as a nutrient for bacteria. We employed a Gram-negative sepsis model and found that elevated heme levels impaired the control of bacterial proliferation independently of heme-iron acquisition by pathogens. Heme strongly inhibited phagocytosis and the migration of human and mouse phagocytes by disrupting actin cytoskeletal dynamics via activation of the GTP-binding Rho family protein Cdc42 by the guanine nucleotide exchange factor DOCK8. A chemical screening approach revealed that quinine effectively prevented heme effects on the cytoskeleton, restored phagocytosis and improved survival in sepsis. These mechanistic insights provide potential therapeutic targets for patients with sepsis or hemolytic disorders.","lang":"eng"}],"day":"01","doi":"10.1038/ni.3590","quality_controlled":"1","page":"1361 - 1372","publisher":"Nature Publishing Group","issue":"12","author":[{"last_name":"Martins","first_name":"Rui","full_name":"Martins, Rui"},{"last_name":"Maier","first_name":"Julia","full_name":"Maier, Julia"},{"full_name":"Gorki, Anna","first_name":"Anna","last_name":"Gorki"},{"full_name":"Huber, Kilian","last_name":"Huber","first_name":"Kilian"},{"last_name":"Sharif","first_name":"Omar","full_name":"Sharif, Omar"},{"full_name":"Starkl, Philipp","last_name":"Starkl","first_name":"Philipp"},{"full_name":"Saluzzo, Simona","first_name":"Simona","last_name":"Saluzzo"},{"first_name":"Federica","last_name":"Quattrone","full_name":"Quattrone, Federica"},{"full_name":"Gawish, Riem","last_name":"Gawish","first_name":"Riem"},{"last_name":"Lakovits","first_name":"Karin","full_name":"Lakovits, Karin"},{"full_name":"Aichinger, Michael","last_name":"Aichinger","first_name":"Michael"},{"last_name":"Radic Sarikas","first_name":"Branka","full_name":"Radic Sarikas, Branka"},{"last_name":"Lardeau","first_name":"Charles","full_name":"Lardeau, Charles"},{"full_name":"Hladik, Anastasiya","last_name":"Hladik","first_name":"Anastasiya"},{"full_name":"Korosec, Ana","last_name":"Korosec","first_name":"Ana"},{"last_name":"Brown","first_name":"Markus","full_name":"Brown, Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87"},{"id":"368EE576-F248-11E8-B48F-1D18A9856A87","full_name":"Vaahtomeri, Kari","orcid":"0000-0001-7829-3518","last_name":"Vaahtomeri","first_name":"Kari"},{"id":"2EDEA62C-F248-11E8-B48F-1D18A9856A87","full_name":"Duggan, Michelle","first_name":"Michelle","last_name":"Duggan"},{"full_name":"Kerjaschki, Dontscho","first_name":"Dontscho","last_name":"Kerjaschki"},{"first_name":"Harald","last_name":"Esterbauer","full_name":"Esterbauer, Harald"},{"full_name":"Colinge, Jacques","first_name":"Jacques","last_name":"Colinge"},{"full_name":"Eisenbarth, Stephanie","last_name":"Eisenbarth","first_name":"Stephanie"},{"last_name":"Decker","first_name":"Thomas","full_name":"Decker, Thomas"},{"full_name":"Bennett, Keiryn","last_name":"Bennett","first_name":"Keiryn"},{"first_name":"Stefan","last_name":"Kubicek","full_name":"Kubicek, Stefan"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt"},{"full_name":"Superti Furga, Giulio","first_name":"Giulio","last_name":"Superti Furga"},{"full_name":"Knapp, Sylvia","first_name":"Sylvia","last_name":"Knapp"}],"scopus_import":1,"_id":"1142","intvolume":"        17","title":"Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions","department":[{"_id":"MiSi"},{"_id":"PeJo"}],"date_created":"2018-12-11T11:50:22Z","publication_status":"published","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","status":"public","main_file_link":[{"url":"https://ora.ox.ac.uk/objects/uuid:f53a464e-1e5b-4f08-a7d8-b6749b852b9d","open_access":"1"}],"type":"journal_article","date_published":"2016-12-01T00:00:00Z","publist_id":"6216","oa":1,"language":[{"iso":"eng"}],"publication":"Nature Immunology","month":"12","oa_version":"Submitted Version"},{"volume":38,"status":"public","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","day":"12","doi":"10.1016/j.devcel.2016.08.017","publist_id":"6208","abstract":[{"lang":"eng","text":"When neutrophils infiltrate a site of inflammation, they have to stop at the right place to exert their effector function. In this issue of Developmental Cell, Wang et al. (2016) show that neutrophils sense reactive oxygen species via the TRPM2 channel to arrest migration at their target site. © 2016 Elsevier Inc."}],"citation":{"ista":"Renkawitz J, Sixt MK. 2016. A Radical Break Restraining Neutrophil Migration. Developmental Cell. 38(5), 448–450.","short":"J. Renkawitz, M.K. Sixt, Developmental Cell 38 (2016) 448–450.","mla":"Renkawitz, Jörg, and Michael K. Sixt. “A Radical Break Restraining Neutrophil Migration.” <i>Developmental Cell</i>, vol. 38, no. 5, Cell Press, 2016, pp. 448–50, doi:<a href=\"https://doi.org/10.1016/j.devcel.2016.08.017\">10.1016/j.devcel.2016.08.017</a>.","ieee":"J. Renkawitz and M. K. Sixt, “A Radical Break Restraining Neutrophil Migration,” <i>Developmental Cell</i>, vol. 38, no. 5. Cell Press, pp. 448–450, 2016.","chicago":"Renkawitz, Jörg, and Michael K Sixt. “A Radical Break Restraining Neutrophil Migration.” <i>Developmental Cell</i>. Cell Press, 2016. <a href=\"https://doi.org/10.1016/j.devcel.2016.08.017\">https://doi.org/10.1016/j.devcel.2016.08.017</a>.","ama":"Renkawitz J, Sixt MK. A Radical Break Restraining Neutrophil Migration. <i>Developmental Cell</i>. 2016;38(5):448-450. doi:<a href=\"https://doi.org/10.1016/j.devcel.2016.08.017\">10.1016/j.devcel.2016.08.017</a>","apa":"Renkawitz, J., &#38; Sixt, M. K. (2016). A Radical Break Restraining Neutrophil Migration. <i>Developmental Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.devcel.2016.08.017\">https://doi.org/10.1016/j.devcel.2016.08.017</a>"},"year":"2016","date_updated":"2021-01-12T06:48:39Z","type":"journal_article","date_published":"2016-09-12T00:00:00Z","publisher":"Cell Press","quality_controlled":"1","page":"448 - 450","language":[{"iso":"eng"}],"date_created":"2018-12-11T11:50:25Z","department":[{"_id":"MiSi"}],"oa_version":"None","publication_status":"published","intvolume":"        38","title":"A Radical Break Restraining Neutrophil Migration","month":"09","scopus_import":1,"_id":"1150","publication":"Developmental Cell","issue":"5","author":[{"first_name":"Jörg","last_name":"Renkawitz","orcid":"0000-0003-2856-3369","full_name":"Renkawitz, Jörg","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}]},{"oa":1,"publist_id":"6204","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"type":"journal_article","date_published":"2016-11-07T00:00:00Z","file":[{"file_name":"IST-2017-744-v1+1_srep36440.pdf","content_type":"application/pdf","date_updated":"2018-12-12T10:09:32Z","file_size":2353456,"date_created":"2018-12-12T10:09:32Z","creator":"system","file_id":"4756","relation":"main_file","access_level":"open_access"}],"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","status":"public","project":[{"name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556","call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425"},{"name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12","call_identifier":"FWF","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425"}],"oa_version":"Published Version","article_number":"36440","month":"11","has_accepted_license":"1","publication":"Scientific Reports","language":[{"iso":"eng"}],"day":"07","doi":"10.1038/srep36440","abstract":[{"text":"Cellular locomotion is a central hallmark of eukaryotic life. It is governed by cell-extrinsic molecular factors, which can either emerge in the soluble phase or as immobilized, often adhesive ligands. To encode for direction, every cue must be present as a spatial or temporal gradient. Here, we developed a microfluidic chamber that allows measurement of cell migration in combined response to surface immobilized and soluble molecular gradients. As a proof of principle we study the response of dendritic cells to their major guidance cues, chemokines. The majority of data on chemokine gradient sensing is based on in vitro studies employing soluble gradients. Despite evidence suggesting that in vivo chemokines are often immobilized to sugar residues, limited information is available how cells respond to immobilized chemokines. We tracked migration of dendritic cells towards immobilized gradients of the chemokine CCL21 and varying superimposed soluble gradients of CCL19. Differential migratory patterns illustrate the potential of our setup to quantitatively study the competitive response to both types of gradients. Beyond chemokines our approach is broadly applicable to alternative systems of chemo- and haptotaxis such as cells migrating along gradients of adhesion receptor ligands vs. any soluble cue. \r\n","lang":"eng"}],"citation":{"short":"J. Schwarz, V. Bierbaum, J. Merrin, T. Frank, R. Hauschild, M.T. Bollenbach, S. Tay, M.K. Sixt, M. Mehling, Scientific Reports 6 (2016).","mla":"Schwarz, Jan, et al. “A Microfluidic Device for Measuring Cell Migration towards Substrate Bound and Soluble Chemokine Gradients.” <i>Scientific Reports</i>, vol. 6, 36440, Nature Publishing Group, 2016, doi:<a href=\"https://doi.org/10.1038/srep36440\">10.1038/srep36440</a>.","ista":"Schwarz J, Bierbaum V, Merrin J, Frank T, Hauschild R, Bollenbach MT, Tay S, Sixt MK, Mehling M. 2016. A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients. Scientific Reports. 6, 36440.","apa":"Schwarz, J., Bierbaum, V., Merrin, J., Frank, T., Hauschild, R., Bollenbach, M. T., … Mehling, M. (2016). A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients. <i>Scientific Reports</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/srep36440\">https://doi.org/10.1038/srep36440</a>","ama":"Schwarz J, Bierbaum V, Merrin J, et al. A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients. <i>Scientific Reports</i>. 2016;6. doi:<a href=\"https://doi.org/10.1038/srep36440\">10.1038/srep36440</a>","chicago":"Schwarz, Jan, Veronika Bierbaum, Jack Merrin, Tino Frank, Robert Hauschild, Mark Tobias Bollenbach, Savaş Tay, Michael K Sixt, and Matthias Mehling. “A Microfluidic Device for Measuring Cell Migration towards Substrate Bound and Soluble Chemokine Gradients.” <i>Scientific Reports</i>. Nature Publishing Group, 2016. <a href=\"https://doi.org/10.1038/srep36440\">https://doi.org/10.1038/srep36440</a>.","ieee":"J. Schwarz <i>et al.</i>, “A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients,” <i>Scientific Reports</i>, vol. 6. Nature Publishing Group, 2016."},"year":"2016","date_updated":"2021-01-12T06:48:41Z","acknowledgement":"This work was supported by the Swiss National Science Foundation (Ambizione fellowship; PZ00P3-154733 to M.M.), the Swiss Multiple Sclerosis Society (research support to M.M.), a fellowship from the Boehringer Ingelheim Fonds (BIF) to J.S., the European Research Council (grant ERC GA 281556) and a START award from the Austrian Science Foundation (FWF) to M.S. #BioimagingFacility","volume":6,"ddc":["579"],"date_created":"2018-12-11T11:50:27Z","department":[{"_id":"MiSi"},{"_id":"NanoFab"},{"_id":"Bio"},{"_id":"ToBo"}],"publication_status":"published","intvolume":"         6","title":"A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients","pubrep_id":"744","scopus_import":1,"_id":"1154","author":[{"last_name":"Schwarz","first_name":"Jan","full_name":"Schwarz, Jan","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Bierbaum, Veronika","last_name":"Bierbaum","first_name":"Veronika","id":"3FD04378-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Jack","last_name":"Merrin","orcid":"0000-0001-5145-4609","full_name":"Merrin, Jack","id":"4515C308-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Frank","first_name":"Tino","full_name":"Frank, Tino"},{"first_name":"Robert","last_name":"Hauschild","orcid":"0000-0001-9843-3522","full_name":"Hauschild, Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87"},{"id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","first_name":"Mark Tobias","last_name":"Bollenbach","orcid":"0000-0003-4398-476X","full_name":"Bollenbach, Mark Tobias"},{"full_name":"Tay, Savaş","first_name":"Savaş","last_name":"Tay"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"id":"3C23B994-F248-11E8-B48F-1D18A9856A87","first_name":"Matthias","last_name":"Mehling","orcid":"0000-0001-8599-1226","full_name":"Mehling, Matthias"}],"publisher":"Nature Publishing Group","ec_funded":1,"quality_controlled":"1","file_date_updated":"2018-12-12T10:09:32Z"},{"file":[{"date_updated":"2020-07-14T12:44:58Z","file_name":"IST-2016-515-v1+1_1-s2.0-S2211124716300262-main.pdf","content_type":"application/pdf","date_created":"2018-12-12T10:12:30Z","checksum":"c98c1151d5f1e5ce1643a83d8d7f3c29","file_size":5489897,"file_id":"4948","creator":"system","access_level":"open_access","relation":"main_file"}],"status":"public","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","oa":1,"publist_id":"5697","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","image":"/images/cc_by_nc_nd.png"},"type":"journal_article","date_published":"2016-02-23T00:00:00Z","language":[{"iso":"eng"}],"oa_version":"Published Version","month":"02","has_accepted_license":"1","publication":"Cell Reports","volume":14,"ddc":["570"],"day":"23","doi":"10.1016/j.celrep.2016.01.048","abstract":[{"lang":"eng","text":"To induce adaptive immunity, dendritic cells (DCs) migrate through afferent lymphatic vessels (LVs) to draining lymph nodes (dLNs). This process occurs in several consecutive steps. Upon entry into lymphatic capillaries, DCs first actively crawl into downstream collecting vessels. From there, they are next passively and rapidly transported to the dLN by lymph flow. Here, we describe a role for the chemokine CCL21 in intralymphatic DC crawling. Performing time-lapse imaging in murine skin, we found that blockade of CCL21-but not the absence of lymph flow-completely abolished DC migration from capillaries toward collecting vessels and reduced the ability of intralymphatic DCs to emigrate from skin. Moreover, we found that in vitro low laminar flow established a CCL21 gradient along lymphatic endothelial monolayers, thereby inducing downstream-directed DC migration. These findings reveal a role for intralymphatic CCL21 in promoting DC trafficking to dLNs, through the formation of a flow-induced gradient."}],"year":"2016","citation":{"ista":"Russo E, Teijeira A, Vaahtomeri K, Willrodt A, Bloch J, Nitschké M, Santambrogio L, Kerjaschki D, Sixt MK, Halin C. 2016. Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels. Cell Reports. 14(7), 1723–1734.","short":"E. Russo, A. Teijeira, K. Vaahtomeri, A. Willrodt, J. Bloch, M. Nitschké, L. Santambrogio, D. Kerjaschki, M.K. Sixt, C. Halin, Cell Reports 14 (2016) 1723–1734.","mla":"Russo, Erica, et al. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic Cells through Afferent Lymphatic Vessels.” <i>Cell Reports</i>, vol. 14, no. 7, Cell Press, 2016, pp. 1723–34, doi:<a href=\"https://doi.org/10.1016/j.celrep.2016.01.048\">10.1016/j.celrep.2016.01.048</a>.","ieee":"E. Russo <i>et al.</i>, “Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels,” <i>Cell Reports</i>, vol. 14, no. 7. Cell Press, pp. 1723–1734, 2016.","chicago":"Russo, Erica, Alvaro Teijeira, Kari Vaahtomeri, Ann Willrodt, Joël Bloch, Maximilian Nitschké, Laura Santambrogio, Dontscho Kerjaschki, Michael K Sixt, and Cornelia Halin. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic Cells through Afferent Lymphatic Vessels.” <i>Cell Reports</i>. Cell Press, 2016. <a href=\"https://doi.org/10.1016/j.celrep.2016.01.048\">https://doi.org/10.1016/j.celrep.2016.01.048</a>.","ama":"Russo E, Teijeira A, Vaahtomeri K, et al. Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels. <i>Cell Reports</i>. 2016;14(7):1723-1734. doi:<a href=\"https://doi.org/10.1016/j.celrep.2016.01.048\">10.1016/j.celrep.2016.01.048</a>","apa":"Russo, E., Teijeira, A., Vaahtomeri, K., Willrodt, A., Bloch, J., Nitschké, M., … Halin, C. (2016). Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels. <i>Cell Reports</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.celrep.2016.01.048\">https://doi.org/10.1016/j.celrep.2016.01.048</a>"},"date_updated":"2021-01-12T06:51:07Z","publisher":"Cell Press","quality_controlled":"1","page":"1723 - 1734","file_date_updated":"2020-07-14T12:44:58Z","department":[{"_id":"MiSi"}],"date_created":"2018-12-11T11:52:19Z","publication_status":"published","intvolume":"        14","pubrep_id":"515","title":"Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels","scopus_import":1,"_id":"1490","issue":"7","author":[{"full_name":"Russo, Erica","first_name":"Erica","last_name":"Russo"},{"last_name":"Teijeira","first_name":"Alvaro","full_name":"Teijeira, Alvaro"},{"first_name":"Kari","last_name":"Vaahtomeri","orcid":"0000-0001-7829-3518","full_name":"Vaahtomeri, Kari","id":"368EE576-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Willrodt, Ann","last_name":"Willrodt","first_name":"Ann"},{"last_name":"Bloch","first_name":"Joël","full_name":"Bloch, Joël"},{"last_name":"Nitschké","first_name":"Maximilian","full_name":"Nitschké, Maximilian"},{"full_name":"Santambrogio, Laura","first_name":"Laura","last_name":"Santambrogio"},{"first_name":"Dontscho","last_name":"Kerjaschki","full_name":"Kerjaschki, Dontscho"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Halin, Cornelia","last_name":"Halin","first_name":"Cornelia"}]},{"page":"567 - 581","ec_funded":1,"quality_controlled":"1","publisher":"Elsevier","article_type":"original","_id":"1597","pmid":1,"scopus_import":1,"author":[{"last_name":"Schwarz","first_name":"Jan","full_name":"Schwarz, Jan","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"publication_status":"published","article_processing_charge":"No","department":[{"_id":"MiSi"}],"date_created":"2018-12-11T11:52:56Z","title":"Quantitative analysis of dendritic cell haptotaxis","intvolume":"       570","volume":570,"acknowledgement":"This work was supported by the Boehringer Ingelheim Fonds, the European Research Council (ERC StG 281556), and a START Award of the Austrian Science Foundation (FWF). We thank Robert Hauschild, Anne Reversat, and Jack Merrin for valuable input and the Imaging Facility of IST Austria for excellent support.","date_updated":"2021-01-12T06:51:51Z","year":"2016","citation":{"short":"J. Schwarz, M.K. Sixt, Methods in Enzymology 570 (2016) 567–581.","mla":"Schwarz, Jan, and Michael K. Sixt. “Quantitative Analysis of Dendritic Cell Haptotaxis.” <i>Methods in Enzymology</i>, vol. 570, Elsevier, 2016, pp. 567–81, doi:<a href=\"https://doi.org/10.1016/bs.mie.2015.11.004\">10.1016/bs.mie.2015.11.004</a>.","ista":"Schwarz J, Sixt MK. 2016. Quantitative analysis of dendritic cell haptotaxis. Methods in Enzymology. 570, 567–581.","apa":"Schwarz, J., &#38; Sixt, M. K. (2016). Quantitative analysis of dendritic cell haptotaxis. <i>Methods in Enzymology</i>. Elsevier. <a href=\"https://doi.org/10.1016/bs.mie.2015.11.004\">https://doi.org/10.1016/bs.mie.2015.11.004</a>","ama":"Schwarz J, Sixt MK. Quantitative analysis of dendritic cell haptotaxis. <i>Methods in Enzymology</i>. 2016;570:567-581. doi:<a href=\"https://doi.org/10.1016/bs.mie.2015.11.004\">10.1016/bs.mie.2015.11.004</a>","ieee":"J. Schwarz and M. K. Sixt, “Quantitative analysis of dendritic cell haptotaxis,” <i>Methods in Enzymology</i>, vol. 570. Elsevier, pp. 567–581, 2016.","chicago":"Schwarz, Jan, and Michael K Sixt. “Quantitative Analysis of Dendritic Cell Haptotaxis.” <i>Methods in Enzymology</i>. Elsevier, 2016. <a href=\"https://doi.org/10.1016/bs.mie.2015.11.004\">https://doi.org/10.1016/bs.mie.2015.11.004</a>."},"external_id":{"pmid":["26921962"]},"doi":"10.1016/bs.mie.2015.11.004","day":"01","abstract":[{"lang":"eng","text":"Chemokines are the main guidance cues directing leukocyte migration. Opposed to early assumptions, chemokines do not necessarily act as soluble cues but are often immobilized within tissues, e.g., dendritic cell migration toward lymphatic vessels is guided by a haptotactic gradient of the chemokine CCL21. Controlled assay systems to quantitatively study haptotaxis in vitro are still missing. In this chapter, we describe an in vitro haptotaxis assay optimized for the unique properties of dendritic cells. The chemokine CCL21 is immobilized in a bioactive state, using laser-assisted protein adsorption by photobleaching. The cells follow this immobilized CCL21 gradient in a haptotaxis chamber, which provides three dimensionally confined migration conditions."}],"language":[{"iso":"eng"}],"publication":"Methods in Enzymology","acknowledged_ssus":[{"_id":"Bio"}],"oa_version":"None","project":[{"call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","grant_number":"281556","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)"},{"name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12","call_identifier":"FWF","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425"}],"month":"01","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","date_published":"2016-01-01T00:00:00Z","type":"journal_article","publist_id":"5573"},{"external_id":{"pmid":["26657283"]},"year":"2016","citation":{"ista":"Kiermaier E, Moussion C, Veldkamp C, Gerardy  Schahn R, de Vries I, Williams L, Chaffee G, Phillips A, Freiberger F, Imre R, Taleski D, Payne R, Braun A, Förster R, Mechtler K, Mühlenhoff M, Volkman B, Sixt MK. 2016. Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. Science. 351(6269), 186–190.","short":"E. Kiermaier, C. Moussion, C. Veldkamp, R. Gerardy  Schahn, I. de Vries, L. Williams, G. Chaffee, A. Phillips, F. Freiberger, R. Imre, D. Taleski, R. Payne, A. Braun, R. Förster, K. Mechtler, M. Mühlenhoff, B. Volkman, M.K. Sixt, Science 351 (2016) 186–190.","mla":"Kiermaier, Eva, et al. “Polysialylation Controls Dendritic Cell Trafficking by Regulating Chemokine Recognition.” <i>Science</i>, vol. 351, no. 6269, American Association for the Advancement of Science, 2016, pp. 186–90, doi:<a href=\"https://doi.org/10.1126/science.aad0512\">10.1126/science.aad0512</a>.","chicago":"Kiermaier, Eva, Christine Moussion, Christopher Veldkamp, Rita Gerardy  Schahn, Ingrid de Vries, Larry Williams, Gary Chaffee, et al. “Polysialylation Controls Dendritic Cell Trafficking by Regulating Chemokine Recognition.” <i>Science</i>. American Association for the Advancement of Science, 2016. <a href=\"https://doi.org/10.1126/science.aad0512\">https://doi.org/10.1126/science.aad0512</a>.","ieee":"E. Kiermaier <i>et al.</i>, “Polysialylation controls dendritic cell trafficking by regulating chemokine recognition,” <i>Science</i>, vol. 351, no. 6269. American Association for the Advancement of Science, pp. 186–190, 2016.","ama":"Kiermaier E, Moussion C, Veldkamp C, et al. Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. <i>Science</i>. 2016;351(6269):186-190. doi:<a href=\"https://doi.org/10.1126/science.aad0512\">10.1126/science.aad0512</a>","apa":"Kiermaier, E., Moussion, C., Veldkamp, C., Gerardy  Schahn, R., de Vries, I., Williams, L., … Sixt, M. K. (2016). Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.aad0512\">https://doi.org/10.1126/science.aad0512</a>"},"date_updated":"2021-01-12T06:51:52Z","abstract":[{"lang":"eng","text":"The addition of polysialic acid to N- and/or O-linked glycans, referred to as polysialylation, is a rare posttranslational modification that is mainly known to control the developmental plasticity of the nervous system. Here we show that CCR7, the central chemokine receptor controlling immune cell trafficking to secondary lymphatic organs, carries polysialic acid. This modification is essential for the recognition of the CCR7 ligand CCL21. As a consequence, dendritic cell trafficking is abrogated in polysialyltransferase-deficient mice, manifesting as disturbed lymph node homeostasis and unresponsiveness to inflammatory stimuli. Structure-function analysis of chemokine-receptor interactions reveals that CCL21 adopts an autoinhibited conformation, which is released upon interaction with polysialic acid. Thus, we describe a glycosylation-mediated immune cell trafficking disorder and its mechanistic basis.\r\n"}],"day":"08","doi":"10.1126/science.aad0512","acknowledgement":"We thank S. Schüchner and E. Ogris for kindly providing the antibody to GFP, M. Helmbrecht and A. Huber for providing Nrp2−/− mice, the IST Scientific Support Facilities for excellent services, and J. Renkawitz and K. Vaahtomeri for critically reading the manuscript. ","volume":351,"issue":"6269","author":[{"orcid":"0000-0001-6165-5738","full_name":"Kiermaier, Eva","first_name":"Eva","last_name":"Kiermaier","id":"3EB04B78-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Moussion","first_name":"Christine","full_name":"Moussion, Christine","id":"3356F664-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Veldkamp, Christopher","last_name":"Veldkamp","first_name":"Christopher"},{"last_name":"Gerardy  Schahn","first_name":"Rita","full_name":"Gerardy  Schahn, Rita"},{"id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid","last_name":"De Vries","full_name":"De Vries, Ingrid"},{"full_name":"Williams, Larry","first_name":"Larry","last_name":"Williams"},{"full_name":"Chaffee, Gary","last_name":"Chaffee","first_name":"Gary"},{"last_name":"Phillips","first_name":"Andrew","full_name":"Phillips, Andrew"},{"full_name":"Freiberger, Friedrich","last_name":"Freiberger","first_name":"Friedrich"},{"first_name":"Richard","last_name":"Imre","full_name":"Imre, Richard"},{"first_name":"Deni","last_name":"Taleski","full_name":"Taleski, Deni"},{"full_name":"Payne, Richard","first_name":"Richard","last_name":"Payne"},{"first_name":"Asolina","last_name":"Braun","full_name":"Braun, Asolina"},{"full_name":"Förster, Reinhold","last_name":"Förster","first_name":"Reinhold"},{"full_name":"Mechtler, Karl","last_name":"Mechtler","first_name":"Karl"},{"full_name":"Mühlenhoff, Martina","first_name":"Martina","last_name":"Mühlenhoff"},{"first_name":"Brian","last_name":"Volkman","full_name":"Volkman, Brian"},{"first_name":"Michael K","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"scopus_import":1,"pmid":1,"_id":"1599","intvolume":"       351","title":"Polysialylation controls dendritic cell trafficking by regulating chemokine recognition","date_created":"2018-12-11T11:52:57Z","department":[{"_id":"MiSi"}],"article_processing_charge":"No","publication_status":"published","ec_funded":1,"quality_controlled":"1","page":"186 - 190","article_type":"original","publisher":"American Association for the Advancement of Science","type":"journal_article","date_published":"2016-01-08T00:00:00Z","publist_id":"5570","oa":1,"status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5583642/"}],"publication":"Science","month":"01","project":[{"call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556"},{"name":"Stromal Cell-immune Cell Interactions in Health and Disease","grant_number":"289720","_id":"25A76F58-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12"}],"acknowledged_ssus":[{"_id":"SSU"}],"oa_version":"Submitted Version","language":[{"iso":"eng"}]},{"acknowledgement":"This work was supported by the German Research Foundation (DFG) Priority Program SP 1464 to T.E.B.S. and M.S., and European Research Council (ERC GA 281556) and Human Frontiers Program grants to M.S.\r\nService Units of IST Austria for excellent technical support.","volume":18,"ddc":["570"],"citation":{"ama":"Leithner AF, Eichner A, Müller J, et al. Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. <i>Nature Cell Biology</i>. 2016;18:1253-1259. doi:<a href=\"https://doi.org/10.1038/ncb3426\">10.1038/ncb3426</a>","apa":"Leithner, A. F., Eichner, A., Müller, J., Reversat, A., Brown, M., Schwarz, J., … Sixt, M. K. (2016). Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. <i>Nature Cell Biology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/ncb3426\">https://doi.org/10.1038/ncb3426</a>","chicago":"Leithner, Alexander F, Alexander Eichner, Jan Müller, Anne Reversat, Markus Brown, Jan Schwarz, Jack Merrin, et al. “Diversified Actin Protrusions Promote Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” <i>Nature Cell Biology</i>. Nature Publishing Group, 2016. <a href=\"https://doi.org/10.1038/ncb3426\">https://doi.org/10.1038/ncb3426</a>.","ieee":"A. F. Leithner <i>et al.</i>, “Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes,” <i>Nature Cell Biology</i>, vol. 18. Nature Publishing Group, pp. 1253–1259, 2016.","short":"A.F. Leithner, A. Eichner, J. Müller, A. Reversat, M. Brown, J. Schwarz, J. Merrin, D. De Gorter, F.K. Schur, J. Bayerl, I. de Vries, S. Wieser, R. Hauschild, F. Lai, M. Moser, D. Kerjaschki, K. Rottner, V. Small, T. Stradal, M.K. Sixt, Nature Cell Biology 18 (2016) 1253–1259.","mla":"Leithner, Alexander F., et al. “Diversified Actin Protrusions Promote Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” <i>Nature Cell Biology</i>, vol. 18, Nature Publishing Group, 2016, pp. 1253–59, doi:<a href=\"https://doi.org/10.1038/ncb3426\">10.1038/ncb3426</a>.","ista":"Leithner AF, Eichner A, Müller J, Reversat A, Brown M, Schwarz J, Merrin J, De Gorter D, Schur FK, Bayerl J, de Vries I, Wieser S, Hauschild R, Lai F, Moser M, Kerjaschki D, Rottner K, Small V, Stradal T, Sixt MK. 2016. Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. 18, 1253–1259."},"year":"2016","date_updated":"2024-03-25T23:30:09Z","day":"24","doi":"10.1038/ncb3426","abstract":[{"lang":"eng","text":"Most migrating cells extrude their front by the force of actin polymerization. Polymerization requires an initial nucleation step, which is mediated by factors establishing either parallel filaments in the case of filopodia or branched filaments that form the branched lamellipodial network. Branches are considered essential for regular cell motility and are initiated by the Arp2/3 complex, which in turn is activated by nucleation-promoting factors of the WASP and WAVE families. Here we employed rapid amoeboid crawling leukocytes and found that deletion of the WAVE complex eliminated actin branching and thus lamellipodia formation. The cells were left with parallel filaments at the leading edge, which translated, depending on the differentiation status of the cell, into a unipolar pointed cell shape or cells with multiple filopodia. Remarkably, unipolar cells migrated with increased speed and enormous directional persistence, while they were unable to turn towards chemotactic gradients. Cells with multiple filopodia retained chemotactic activity but their migration was progressively impaired with increasing geometrical complexity of the extracellular environment. These findings establish that diversified leading edge protrusions serve as explorative structures while they slow down actual locomotion."}],"ec_funded":1,"quality_controlled":"1","page":"1253 - 1259","file_date_updated":"2020-07-14T12:44:43Z","publisher":"Nature Publishing Group","article_type":"original","scopus_import":1,"_id":"1321","author":[{"full_name":"Leithner, Alexander F","orcid":"0000-0002-1073-744X","last_name":"Leithner","first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87"},{"id":"4DFA52AE-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander","last_name":"Eichner","full_name":"Eichner, Alexander"},{"first_name":"Jan","last_name":"Müller","full_name":"Müller, Jan","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D"},{"id":"35B76592-F248-11E8-B48F-1D18A9856A87","last_name":"Reversat","first_name":"Anne","full_name":"Reversat, Anne","orcid":"0000-0003-0666-8928"},{"id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","full_name":"Brown, Markus","first_name":"Markus","last_name":"Brown"},{"first_name":"Jan","last_name":"Schwarz","full_name":"Schwarz, Jan","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Merrin, Jack","orcid":"0000-0001-5145-4609","last_name":"Merrin","first_name":"Jack","id":"4515C308-F248-11E8-B48F-1D18A9856A87"},{"full_name":"De Gorter, David","last_name":"De Gorter","first_name":"David"},{"full_name":"Schur, Florian","orcid":"0000-0003-4790-8078","last_name":"Schur","first_name":"Florian","id":"48AD8942-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Jonathan","last_name":"Bayerl","full_name":"Bayerl, Jonathan"},{"first_name":"Ingrid","last_name":"De Vries","full_name":"De Vries, Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Wieser, Stefan","orcid":"0000-0002-2670-2217","last_name":"Wieser","first_name":"Stefan","id":"355AA5A0-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Robert","last_name":"Hauschild","orcid":"0000-0001-9843-3522","full_name":"Hauschild, Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Frank","last_name":"Lai","full_name":"Lai, Frank"},{"first_name":"Markus","last_name":"Moser","full_name":"Moser, Markus"},{"last_name":"Kerjaschki","first_name":"Dontscho","full_name":"Kerjaschki, Dontscho"},{"last_name":"Rottner","first_name":"Klemens","full_name":"Rottner, Klemens"},{"first_name":"Victor","last_name":"Small","full_name":"Small, Victor"},{"last_name":"Stradal","first_name":"Theresia","full_name":"Stradal, Theresia"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179"}],"date_created":"2018-12-11T11:51:21Z","department":[{"_id":"MiSi"},{"_id":"NanoFab"},{"_id":"Bio"}],"article_processing_charge":"No","publication_status":"published","intvolume":"        18","title":"Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes","file":[{"access_level":"open_access","relation":"main_file","file_id":"7844","creator":"dernst","date_created":"2020-05-14T16:33:46Z","checksum":"e1411cb7c99a2d9089c178a6abef25e7","file_size":4433280,"date_updated":"2020-07-14T12:44:43Z","content_type":"application/pdf","file_name":"2018_NatureCell_Leithner.pdf"}],"related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"323"}]},"status":"public","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","image":"/images/cc_by_nc_sa.png","short":"CC BY-NC-SA (4.0)"},"type":"journal_article","date_published":"2016-10-24T00:00:00Z","publist_id":"5949","oa":1,"language":[{"iso":"eng"}],"has_accepted_license":"1","publication":"Nature Cell Biology","project":[{"call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556"}],"acknowledged_ssus":[{"_id":"SSU"}],"oa_version":"Submitted Version","month":"10"},{"language":[{"iso":"eng"}],"quality_controlled":"1","page":"1448 - 1449","publisher":"Cell Press","issue":"6","author":[{"id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","last_name":"Renkawitz","first_name":"Jörg","full_name":"Renkawitz, Jörg","orcid":"0000-0003-2856-3369"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"}],"scopus_import":1,"publication":"Cell","_id":"1201","intvolume":"       167","month":"12","title":"Formin’ a nuclear protection","date_created":"2018-12-11T11:50:41Z","department":[{"_id":"MiSi"}],"publication_status":"published","oa_version":"None","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","status":"public","volume":167,"type":"journal_article","date_published":"2016-12-01T00:00:00Z","year":"2016","citation":{"ista":"Renkawitz J, Sixt MK. 2016. Formin’ a nuclear protection. Cell. 167(6), 1448–1449.","mla":"Renkawitz, Jörg, and Michael K. Sixt. “Formin’ a Nuclear Protection.” <i>Cell</i>, vol. 167, no. 6, Cell Press, 2016, pp. 1448–49, doi:<a href=\"https://doi.org/10.1016/j.cell.2016.11.024\">10.1016/j.cell.2016.11.024</a>.","short":"J. Renkawitz, M.K. Sixt, Cell 167 (2016) 1448–1449.","chicago":"Renkawitz, Jörg, and Michael K Sixt. “Formin’ a Nuclear Protection.” <i>Cell</i>. Cell Press, 2016. <a href=\"https://doi.org/10.1016/j.cell.2016.11.024\">https://doi.org/10.1016/j.cell.2016.11.024</a>.","ieee":"J. Renkawitz and M. K. Sixt, “Formin’ a nuclear protection,” <i>Cell</i>, vol. 167, no. 6. Cell Press, pp. 1448–1449, 2016.","ama":"Renkawitz J, Sixt MK. Formin’ a nuclear protection. <i>Cell</i>. 2016;167(6):1448-1449. doi:<a href=\"https://doi.org/10.1016/j.cell.2016.11.024\">10.1016/j.cell.2016.11.024</a>","apa":"Renkawitz, J., &#38; Sixt, M. K. (2016). Formin’ a nuclear protection. <i>Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.cell.2016.11.024\">https://doi.org/10.1016/j.cell.2016.11.024</a>"},"date_updated":"2021-01-12T06:49:03Z","publist_id":"6149","abstract":[{"lang":"eng","text":"In this issue of Cell, Skau et al. show that the formin FMN2 organizes a perinuclear actin cytoskeleton that protects the nucleus and its genomic content of migrating cells squeezing through small spaces."}],"day":"01","doi":"10.1016/j.cell.2016.11.024"},{"publication_status":"published","oa_version":"None","date_created":"2018-12-11T11:50:46Z","department":[{"_id":"MiSi"}],"month":"01","title":"Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors","intvolume":"        94","publication":"Immunology and Cell Biology","_id":"1217","scopus_import":1,"author":[{"last_name":"Sreeramkumar","first_name":"Vinatha","full_name":"Sreeramkumar, Vinatha"},{"first_name":"Miroslav","last_name":"Hons","orcid":"0000-0002-6625-3348","full_name":"Hons, Miroslav","id":"4167FE56-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Punzón","first_name":"Carmen","full_name":"Punzón, Carmen"},{"last_name":"Stein","first_name":"Jens","full_name":"Stein, Jens"},{"first_name":"David","last_name":"Sancho","full_name":"Sancho, David"},{"full_name":"Fresno Forcelledo, Manuel","first_name":"Manuel","last_name":"Fresno Forcelledo"},{"full_name":"Cuesta, Natalia","first_name":"Natalia","last_name":"Cuesta"}],"issue":"1","publisher":"Nature Publishing Group","page":"39 - 51","quality_controlled":"1","language":[{"iso":"eng"}],"doi":"10.1038/icb.2015.62","day":"01","abstract":[{"lang":"eng","text":"Understanding the regulation of T-cell responses during inflammation and auto-immunity is fundamental for designing efficient therapeutic strategies against immune diseases. In this regard, prostaglandin E 2 (PGE 2) is mostly considered a myeloid-derived immunosuppressive molecule. We describe for the first time that T cells secrete PGE 2 during T-cell receptor stimulation. In addition, we show that autocrine PGE 2 signaling through EP receptors is essential for optimal CD4 + T-cell activation in vitro and in vivo, and for T helper 1 (Th1) and regulatory T cell differentiation. PGE 2 was found to provide additive co-stimulatory signaling through AKT activation. Intravital multiphoton microscopy showed that triggering EP receptors in T cells is also essential for the stability of T cell-dendritic cell (DC) interactions and Th-cell accumulation in draining lymph nodes (LNs) during inflammation. We further demonstrated that blocking EP receptors in T cells during the initial phase of collagen-induced arthritis in mice resulted in a reduction of clinical arthritis. This could be attributable to defective T-cell activation, accompanied by a decline in activated and interferon-γ-producing CD4 + Th1 cells in draining LNs. In conclusion, we prove that T lymphocytes secret picomolar concentrations of PGE 2, which in turn provide additive co-stimulatory signaling, enabling T cells to attain a favorable activation threshold. PGE 2 signaling in T cells is also required for maintaining long and stable interactions with DCs within LNs. Blockade of EP receptors in vivo impairs T-cell activation and development of T cell-mediated inflammatory responses. This may have implications in various pathophysiological settings."}],"publist_id":"6116","date_updated":"2021-01-12T06:49:09Z","citation":{"ama":"Sreeramkumar V, Hons M, Punzón C, et al. Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors. <i>Immunology and Cell Biology</i>. 2016;94(1):39-51. doi:<a href=\"https://doi.org/10.1038/icb.2015.62\">10.1038/icb.2015.62</a>","apa":"Sreeramkumar, V., Hons, M., Punzón, C., Stein, J., Sancho, D., Fresno Forcelledo, M., &#38; Cuesta, N. (2016). Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors. <i>Immunology and Cell Biology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/icb.2015.62\">https://doi.org/10.1038/icb.2015.62</a>","chicago":"Sreeramkumar, Vinatha, Miroslav Hons, Carmen Punzón, Jens Stein, David Sancho, Manuel Fresno Forcelledo, and Natalia Cuesta. “Efficient T-Cell Priming and Activation Requires Signaling through Prostaglandin E2 (EP) Receptors.” <i>Immunology and Cell Biology</i>. Nature Publishing Group, 2016. <a href=\"https://doi.org/10.1038/icb.2015.62\">https://doi.org/10.1038/icb.2015.62</a>.","ieee":"V. Sreeramkumar <i>et al.</i>, “Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors,” <i>Immunology and Cell Biology</i>, vol. 94, no. 1. Nature Publishing Group, pp. 39–51, 2016.","mla":"Sreeramkumar, Vinatha, et al. “Efficient T-Cell Priming and Activation Requires Signaling through Prostaglandin E2 (EP) Receptors.” <i>Immunology and Cell Biology</i>, vol. 94, no. 1, Nature Publishing Group, 2016, pp. 39–51, doi:<a href=\"https://doi.org/10.1038/icb.2015.62\">10.1038/icb.2015.62</a>.","short":"V. Sreeramkumar, M. Hons, C. Punzón, J. Stein, D. Sancho, M. Fresno Forcelledo, N. Cuesta, Immunology and Cell Biology 94 (2016) 39–51.","ista":"Sreeramkumar V, Hons M, Punzón C, Stein J, Sancho D, Fresno Forcelledo M, Cuesta N. 2016. Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors. Immunology and Cell Biology. 94(1), 39–51."},"year":"2016","date_published":"2016-01-01T00:00:00Z","type":"journal_article","acknowledgement":"This manuscript has been supported by grants SAF2007-61716 and S-SAL-0159/2006 awarded by the Spanish Ministry of Science and Education and the Community of Madrid to Dr M Fresno.","volume":94,"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","status":"public"},{"intvolume":"        32","title":"Focal adhesion-independent cell migration","month":"10","date_created":"2018-12-11T11:51:08Z","department":[{"_id":"MiSi"}],"project":[{"call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","grant_number":"281556","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)"},{"name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12","call_identifier":"FWF","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425"}],"oa_version":"None","publication_status":"published","author":[{"last_name":"Paluch","first_name":"Ewa","full_name":"Paluch, Ewa"},{"last_name":"Aspalter","first_name":"Irene","full_name":"Aspalter, Irene"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179"}],"scopus_import":1,"publication":"Annual Review of Cell and Developmental Biology","_id":"1285","publisher":"Annual Reviews","language":[{"iso":"eng"}],"quality_controlled":"1","ec_funded":1,"page":"469 - 490","publist_id":"6031","abstract":[{"lang":"eng","text":"Cell migration is central to a multitude of physiological processes, including embryonic development, immune surveillance, and wound healing, and deregulated migration is key to cancer dissemination. Decades of investigations have uncovered many of the molecular and physical mechanisms underlying cell migration. Together with protrusion extension and cell body retraction, adhesion to the substrate via specific focal adhesion points has long been considered an essential step in cell migration. Although this is true for cells moving on two-dimensional substrates, recent studies have demonstrated that focal adhesions are not required for cells moving in three dimensions, in which confinement is sufficient to maintain a cell in contact with its substrate. Here, we review the investigations that have led to challenging the requirement of specific adhesions for migration, discuss the physical mechanisms proposed for cell body translocation during focal adhesion-independent migration, and highlight the remaining open questions for the future."}],"day":"06","doi":"10.1146/annurev-cellbio-111315-125341","type":"journal_article","date_published":"2016-10-06T00:00:00Z","citation":{"mla":"Paluch, Ewa, et al. “Focal Adhesion-Independent Cell Migration.” <i>Annual Review of Cell and Developmental Biology</i>, vol. 32, Annual Reviews, 2016, pp. 469–90, doi:<a href=\"https://doi.org/10.1146/annurev-cellbio-111315-125341\">10.1146/annurev-cellbio-111315-125341</a>.","short":"E. Paluch, I. Aspalter, M.K. Sixt, Annual Review of Cell and Developmental Biology 32 (2016) 469–490.","ista":"Paluch E, Aspalter I, Sixt MK. 2016. Focal adhesion-independent cell migration. Annual Review of Cell and Developmental Biology. 32, 469–490.","apa":"Paluch, E., Aspalter, I., &#38; Sixt, M. K. (2016). Focal adhesion-independent cell migration. <i>Annual Review of Cell and Developmental Biology</i>. Annual Reviews. <a href=\"https://doi.org/10.1146/annurev-cellbio-111315-125341\">https://doi.org/10.1146/annurev-cellbio-111315-125341</a>","ama":"Paluch E, Aspalter I, Sixt MK. Focal adhesion-independent cell migration. <i>Annual Review of Cell and Developmental Biology</i>. 2016;32:469-490. doi:<a href=\"https://doi.org/10.1146/annurev-cellbio-111315-125341\">10.1146/annurev-cellbio-111315-125341</a>","ieee":"E. Paluch, I. Aspalter, and M. K. Sixt, “Focal adhesion-independent cell migration,” <i>Annual Review of Cell and Developmental Biology</i>, vol. 32. Annual Reviews, pp. 469–490, 2016.","chicago":"Paluch, Ewa, Irene Aspalter, and Michael K Sixt. “Focal Adhesion-Independent Cell Migration.” <i>Annual Review of Cell and Developmental Biology</i>. Annual Reviews, 2016. <a href=\"https://doi.org/10.1146/annurev-cellbio-111315-125341\">https://doi.org/10.1146/annurev-cellbio-111315-125341</a>."},"year":"2016","date_updated":"2021-01-12T06:49:37Z","status":"public","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","volume":32,"acknowledgement":"We would like to thank Dani Bodor for critical comments on the manuscript and Guillaume Salbreux for discussions. The authors are supported by the United Kingdom's Medical Research Council (MRC) (E.K.P. and I.M.A.; core funding to the MRC Laboratory for Molecular Cell Biology), by the European Research Council [ERC GA 311637 (E.K.P.) and ERC GA 281556 (M.S.)], and by a START award from the Austrian Science Foundation (M.S.)."},{"page":"4163 - 4166","quality_controlled":"1","ec_funded":1,"publisher":"American Chemical Society","_id":"1618","pmid":1,"scopus_import":"1","author":[{"last_name":"Veldkamp","first_name":"Christopher","full_name":"Veldkamp, Christopher"},{"id":"3EB04B78-F248-11E8-B48F-1D18A9856A87","last_name":"Kiermaier","first_name":"Eva","full_name":"Kiermaier, Eva","orcid":"0000-0001-6165-5738"},{"full_name":"Gabel Eissens, Skylar","first_name":"Skylar","last_name":"Gabel Eissens"},{"last_name":"Gillitzer","first_name":"Miranda","full_name":"Gillitzer, Miranda"},{"full_name":"Lippner, David","last_name":"Lippner","first_name":"David"},{"full_name":"Disilvio, Frank","first_name":"Frank","last_name":"Disilvio"},{"first_name":"Casey","last_name":"Mueller","full_name":"Mueller, Casey"},{"first_name":"Paeton","last_name":"Wantuch","full_name":"Wantuch, Paeton"},{"full_name":"Chaffee, Gary","first_name":"Gary","last_name":"Chaffee"},{"last_name":"Famiglietti","first_name":"Michael","full_name":"Famiglietti, Michael"},{"full_name":"Zgoba, Danielle","first_name":"Danielle","last_name":"Zgoba"},{"full_name":"Bailey, Asha","last_name":"Bailey","first_name":"Asha"},{"first_name":"Yaya","last_name":"Bah","full_name":"Bah, Yaya"},{"last_name":"Engebretson","first_name":"Samantha","full_name":"Engebretson, Samantha"},{"full_name":"Graupner, David","last_name":"Graupner","first_name":"David"},{"first_name":"Emily","last_name":"Lackner","full_name":"Lackner, Emily"},{"last_name":"Larosa","first_name":"Vincent","full_name":"Larosa, Vincent"},{"first_name":"Tysha","last_name":"Medeiros","full_name":"Medeiros, Tysha"},{"last_name":"Olson","first_name":"Michael","full_name":"Olson, Michael"},{"last_name":"Phillips","first_name":"Andrew","full_name":"Phillips, Andrew"},{"full_name":"Pyles, Harley","last_name":"Pyles","first_name":"Harley"},{"last_name":"Richard","first_name":"Amanda","full_name":"Richard, Amanda"},{"last_name":"Schoeller","first_name":"Scott","full_name":"Schoeller, Scott"},{"first_name":"Boris","last_name":"Touzeau","full_name":"Touzeau, Boris"},{"full_name":"Williams, Larry","first_name":"Larry","last_name":"Williams"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179"},{"full_name":"Peterson, Francis","first_name":"Francis","last_name":"Peterson"}],"issue":"27","publication_status":"published","department":[{"_id":"MiSi"}],"article_processing_charge":"No","date_created":"2018-12-11T11:53:03Z","title":"Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites","intvolume":"        54","volume":54,"date_updated":"2023-03-30T11:32:57Z","citation":{"ama":"Veldkamp C, Kiermaier E, Gabel Eissens S, et al. Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites. <i>Biochemistry</i>. 2015;54(27):4163-4166. doi:<a href=\"https://doi.org/10.1021/acs.biochem.5b00560\">10.1021/acs.biochem.5b00560</a>","apa":"Veldkamp, C., Kiermaier, E., Gabel Eissens, S., Gillitzer, M., Lippner, D., Disilvio, F., … Peterson, F. (2015). Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites. <i>Biochemistry</i>. American Chemical Society. <a href=\"https://doi.org/10.1021/acs.biochem.5b00560\">https://doi.org/10.1021/acs.biochem.5b00560</a>","chicago":"Veldkamp, Christopher, Eva Kiermaier, Skylar Gabel Eissens, Miranda Gillitzer, David Lippner, Frank Disilvio, Casey Mueller, et al. “Solution Structure of CCL19 and Identification of Overlapping CCR7 and PSGL-1 Binding Sites.” <i>Biochemistry</i>. American Chemical Society, 2015. <a href=\"https://doi.org/10.1021/acs.biochem.5b00560\">https://doi.org/10.1021/acs.biochem.5b00560</a>.","ieee":"C. Veldkamp <i>et al.</i>, “Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites,” <i>Biochemistry</i>, vol. 54, no. 27. American Chemical Society, pp. 4163–4166, 2015.","short":"C. Veldkamp, E. Kiermaier, S. Gabel Eissens, M. Gillitzer, D. Lippner, F. Disilvio, C. Mueller, P. Wantuch, G. Chaffee, M. Famiglietti, D. Zgoba, A. Bailey, Y. Bah, S. Engebretson, D. Graupner, E. Lackner, V. Larosa, T. Medeiros, M. Olson, A. Phillips, H. Pyles, A. Richard, S. Schoeller, B. Touzeau, L. Williams, M.K. Sixt, F. Peterson, Biochemistry 54 (2015) 4163–4166.","mla":"Veldkamp, Christopher, et al. “Solution Structure of CCL19 and Identification of Overlapping CCR7 and PSGL-1 Binding Sites.” <i>Biochemistry</i>, vol. 54, no. 27, American Chemical Society, 2015, pp. 4163–66, doi:<a href=\"https://doi.org/10.1021/acs.biochem.5b00560\">10.1021/acs.biochem.5b00560</a>.","ista":"Veldkamp C, Kiermaier E, Gabel Eissens S, Gillitzer M, Lippner D, Disilvio F, Mueller C, Wantuch P, Chaffee G, Famiglietti M, Zgoba D, Bailey A, Bah Y, Engebretson S, Graupner D, Lackner E, Larosa V, Medeiros T, Olson M, Phillips A, Pyles H, Richard A, Schoeller S, Touzeau B, Williams L, Sixt MK, Peterson F. 2015. Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites. Biochemistry. 54(27), 4163–4166."},"year":"2015","external_id":{"pmid":["26115234"]},"doi":"10.1021/acs.biochem.5b00560","day":"26","abstract":[{"lang":"eng","text":"CCL19 and CCL21 are chemokines involved in the trafficking of immune cells, particularly within the lymphatic system, through activation of CCR7. Concurrent expression of PSGL-1 and CCR7 in naive T-cells enhances recruitment of these cells to secondary lymphoid organs by CCL19 and CCL21. Here the solution structure of CCL19 is reported. It contains a canonical chemokine domain. Chemical shift mapping shows the N-termini of PSGL-1 and CCR7 have overlapping binding sites for CCL19 and binding is competitive. Implications for the mechanism of PSGL-1's enhancement of resting T-cell recruitment are discussed."}],"language":[{"iso":"eng"}],"publication":"Biochemistry","oa_version":"Submitted Version","project":[{"call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556"}],"month":"06","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4809050/"}],"status":"public","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","date_published":"2015-06-26T00:00:00Z","type":"journal_article","publist_id":"5548","oa":1},{"volume":36,"status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","day":"01","doi":"10.1016/j.ceb.2015.09.004","publist_id":"5473","year":"2015","citation":{"ama":"Sixt MK, Raz E. Editorial overview: Cell adhesion and migration. <i>Current Opinion in Cell Biology</i>. 2015;36(10):4-6. doi:<a href=\"https://doi.org/10.1016/j.ceb.2015.09.004\">10.1016/j.ceb.2015.09.004</a>","apa":"Sixt, M. K., &#38; Raz, E. (2015). Editorial overview: Cell adhesion and migration. <i>Current Opinion in Cell Biology</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.ceb.2015.09.004\">https://doi.org/10.1016/j.ceb.2015.09.004</a>","chicago":"Sixt, Michael K, and Erez Raz. “Editorial Overview: Cell Adhesion and Migration.” <i>Current Opinion in Cell Biology</i>. Elsevier, 2015. <a href=\"https://doi.org/10.1016/j.ceb.2015.09.004\">https://doi.org/10.1016/j.ceb.2015.09.004</a>.","ieee":"M. K. Sixt and E. Raz, “Editorial overview: Cell adhesion and migration,” <i>Current Opinion in Cell Biology</i>, vol. 36, no. 10. Elsevier, pp. 4–6, 2015.","short":"M.K. Sixt, E. Raz, Current Opinion in Cell Biology 36 (2015) 4–6.","mla":"Sixt, Michael K., and Erez Raz. “Editorial Overview: Cell Adhesion and Migration.” <i>Current Opinion in Cell Biology</i>, vol. 36, no. 10, Elsevier, 2015, pp. 4–6, doi:<a href=\"https://doi.org/10.1016/j.ceb.2015.09.004\">10.1016/j.ceb.2015.09.004</a>.","ista":"Sixt MK, Raz E. 2015. Editorial overview: Cell adhesion and migration. Current Opinion in Cell Biology. 36(10), 4–6."},"date_updated":"2021-01-12T06:52:27Z","type":"journal_article","date_published":"2015-10-01T00:00:00Z","publisher":"Elsevier","page":"4 - 6","language":[{"iso":"eng"}],"department":[{"_id":"MiSi"}],"date_created":"2018-12-11T11:53:25Z","publication_status":"published","oa_version":"None","intvolume":"        36","title":"Editorial overview: Cell adhesion and migration","month":"10","scopus_import":1,"_id":"1676","publication":"Current Opinion in Cell Biology","issue":"10","author":[{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt"},{"full_name":"Raz, Erez","last_name":"Raz","first_name":"Erez"}]},{"title":"Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection","month":"09","intvolume":"       349","publication_status":"published","oa_version":"None","date_created":"2018-12-11T11:53:28Z","department":[{"_id":"MiSi"}],"author":[{"id":"3EB04B78-F248-11E8-B48F-1D18A9856A87","first_name":"Eva","last_name":"Kiermaier","orcid":"0000-0001-6165-5738","full_name":"Kiermaier, Eva"},{"full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"issue":"6252","publication":"Science","_id":"1686","scopus_import":1,"publisher":"American Association for the Advancement of Science","language":[{"iso":"eng"}],"page":"1055 - 1056","quality_controlled":"1","publist_id":"5459","doi":"10.1126/science.aad0867","day":"04","date_published":"2015-09-04T00:00:00Z","type":"journal_article","date_updated":"2021-01-12T06:52:31Z","citation":{"mla":"Kiermaier, Eva, and Michael K. Sixt. “Fragmented Communication between Immune Cells: Neutrophils Blaze a Trail with Migratory Cues for T Cells to Follow to Sites of Infection.” <i>Science</i>, vol. 349, no. 6252, American Association for the Advancement of Science, 2015, pp. 1055–56, doi:<a href=\"https://doi.org/10.1126/science.aad0867\">10.1126/science.aad0867</a>.","short":"E. Kiermaier, M.K. Sixt, Science 349 (2015) 1055–1056.","ista":"Kiermaier E, Sixt MK. 2015. Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. Science. 349(6252), 1055–1056.","apa":"Kiermaier, E., &#38; Sixt, M. K. (2015). Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.aad0867\">https://doi.org/10.1126/science.aad0867</a>","ama":"Kiermaier E, Sixt MK. Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. <i>Science</i>. 2015;349(6252):1055-1056. doi:<a href=\"https://doi.org/10.1126/science.aad0867\">10.1126/science.aad0867</a>","ieee":"E. Kiermaier and M. K. Sixt, “Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection,” <i>Science</i>, vol. 349, no. 6252. American Association for the Advancement of Science, pp. 1055–1056, 2015.","chicago":"Kiermaier, Eva, and Michael K Sixt. “Fragmented Communication between Immune Cells: Neutrophils Blaze a Trail with Migratory Cues for T Cells to Follow to Sites of Infection.” <i>Science</i>. American Association for the Advancement of Science, 2015. <a href=\"https://doi.org/10.1126/science.aad0867\">https://doi.org/10.1126/science.aad0867</a>."},"year":"2015","status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","volume":349},{"language":[{"iso":"eng"}],"publication":"Current Opinion in Cell Biology","has_accepted_license":"1","oa_version":"Published Version","project":[{"name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556","call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425"}],"month":"10","file":[{"date_created":"2018-12-12T10:11:21Z","file_size":797964,"checksum":"c29973924b790aab02fdd91857759cfb","date_updated":"2020-07-14T12:45:12Z","content_type":"application/pdf","file_name":"IST-2016-445-v1+1_1-s2.0-S0955067415001064-main.pdf","relation":"main_file","access_level":"open_access","file_id":"4875","creator":"system"}],"status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"date_published":"2015-10-01T00:00:00Z","type":"journal_article","publist_id":"5458","oa":1,"page":"93 - 102","ec_funded":1,"quality_controlled":"1","file_date_updated":"2020-07-14T12:45:12Z","publisher":"Elsevier","_id":"1687","scopus_import":1,"author":[{"full_name":"Sarris, Milka","last_name":"Sarris","first_name":"Milka"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179"}],"issue":"10","publication_status":"published","date_created":"2018-12-11T11:53:28Z","department":[{"_id":"MiSi"}],"pubrep_id":"445","title":"Navigating in tissue mazes: Chemoattractant interpretation in complex environments","intvolume":"        36","volume":36,"ddc":["570"],"date_updated":"2021-01-12T06:52:31Z","citation":{"ista":"Sarris M, Sixt MK. 2015. Navigating in tissue mazes: Chemoattractant interpretation in complex environments. Current Opinion in Cell Biology. 36(10), 93–102.","mla":"Sarris, Milka, and Michael K. Sixt. “Navigating in Tissue Mazes: Chemoattractant Interpretation in Complex Environments.” <i>Current Opinion in Cell Biology</i>, vol. 36, no. 10, Elsevier, 2015, pp. 93–102, doi:<a href=\"https://doi.org/10.1016/j.ceb.2015.08.001\">10.1016/j.ceb.2015.08.001</a>.","short":"M. Sarris, M.K. Sixt, Current Opinion in Cell Biology 36 (2015) 93–102.","ieee":"M. Sarris and M. K. Sixt, “Navigating in tissue mazes: Chemoattractant interpretation in complex environments,” <i>Current Opinion in Cell Biology</i>, vol. 36, no. 10. Elsevier, pp. 93–102, 2015.","chicago":"Sarris, Milka, and Michael K Sixt. “Navigating in Tissue Mazes: Chemoattractant Interpretation in Complex Environments.” <i>Current Opinion in Cell Biology</i>. Elsevier, 2015. <a href=\"https://doi.org/10.1016/j.ceb.2015.08.001\">https://doi.org/10.1016/j.ceb.2015.08.001</a>.","ama":"Sarris M, Sixt MK. Navigating in tissue mazes: Chemoattractant interpretation in complex environments. <i>Current Opinion in Cell Biology</i>. 2015;36(10):93-102. doi:<a href=\"https://doi.org/10.1016/j.ceb.2015.08.001\">10.1016/j.ceb.2015.08.001</a>","apa":"Sarris, M., &#38; Sixt, M. K. (2015). Navigating in tissue mazes: Chemoattractant interpretation in complex environments. <i>Current Opinion in Cell Biology</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.ceb.2015.08.001\">https://doi.org/10.1016/j.ceb.2015.08.001</a>"},"year":"2015","doi":"10.1016/j.ceb.2015.08.001","day":"01","abstract":[{"text":"Guided cell movement is essential for development and integrity of animals and crucially involved in cellular immune responses. Leukocytes are professional migratory cells that can navigate through most types of tissues and sense a wide range of directional cues. The responses of these cells to attractants have been mainly explored in tissue culture settings. How leukocytes make directional decisions in situ, within the challenging environment of a tissue maze, is less understood. Here we review recent advances in how leukocytes sense chemical cues in complex tissue settings and make links with paradigms of directed migration in development and Dictyostelium discoideum amoebae.","lang":"eng"}]},{"citation":{"ieee":"K. Holst <i>et al.</i>, “The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells,” <i>Journal of Cell Science</i>, vol. 128, no. 15. Company of Biologists, pp. 2866–2880, 2015.","chicago":"Holst, Katrin, Daria Guseva, Susann Schindler, Michael K Sixt, Armin Braun, Himpriya Chopra, Oliver Pabst, and Evgeni Ponimaskin. “The Serotonin Receptor 5-HT7R Regulates the Morphology and Migratory Properties of Dendritic Cells.” <i>Journal of Cell Science</i>. Company of Biologists, 2015. <a href=\"https://doi.org/10.1242/jcs.167999\">https://doi.org/10.1242/jcs.167999</a>.","apa":"Holst, K., Guseva, D., Schindler, S., Sixt, M. K., Braun, A., Chopra, H., … Ponimaskin, E. (2015). The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. <i>Journal of Cell Science</i>. Company of Biologists. <a href=\"https://doi.org/10.1242/jcs.167999\">https://doi.org/10.1242/jcs.167999</a>","ama":"Holst K, Guseva D, Schindler S, et al. The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. <i>Journal of Cell Science</i>. 2015;128(15):2866-2880. doi:<a href=\"https://doi.org/10.1242/jcs.167999\">10.1242/jcs.167999</a>","ista":"Holst K, Guseva D, Schindler S, Sixt MK, Braun A, Chopra H, Pabst O, Ponimaskin E. 2015. The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. Journal of Cell Science. 128(15), 2866–2880.","short":"K. Holst, D. Guseva, S. Schindler, M.K. Sixt, A. Braun, H. Chopra, O. Pabst, E. Ponimaskin, Journal of Cell Science 128 (2015) 2866–2880.","mla":"Holst, Katrin, et al. “The Serotonin Receptor 5-HT7R Regulates the Morphology and Migratory Properties of Dendritic Cells.” <i>Journal of Cell Science</i>, vol. 128, no. 15, Company of Biologists, 2015, pp. 2866–80, doi:<a href=\"https://doi.org/10.1242/jcs.167999\">10.1242/jcs.167999</a>."},"year":"2015","date_updated":"2021-01-12T08:00:54Z","type":"journal_article","date_published":"2015-06-15T00:00:00Z","day":"15","doi":"10.1242/jcs.167999","publist_id":"7343","abstract":[{"lang":"eng","text":"Dendritic cells are potent antigen-presenting cells endowed with the unique ability to initiate adaptive immune responses upon inflammation. Inflammatory processes are often associated with an increased production of serotonin, which operates by activating specific receptors. However, the functional role of serotonin receptors in regulation of dendritic cell functions is poorly understood. Here, we demonstrate that expression of serotonin receptor 5-HT7 (5-HT7TR) as well as its downstream effector Cdc42 is upregulated in dendritic cells upon maturation. Although dendritic cell maturation was independent of 5-HT7TR, receptor stimulation affected dendritic cell morphology through Cdc42-mediated signaling. In addition, basal activity of 5-HT7TR was required for the proper expression of the chemokine receptor CCR7, which is a key factor that controls dendritic cell migration. Consistent with this, we observed that 5-HT7TR enhances chemotactic motility of dendritic cells in vitro by modulating their directionality and migration velocity. Accordingly, migration of dendritic cells in murine colon explants was abolished after pharmacological receptor inhibition. Our results indicate that there is a crucial role for 5-HT7TR-Cdc42-mediated signaling in the regulation of dendritic cell morphology and motility, suggesting that 5-HT7TR could be a new target for treatment of a variety of inflammatory and immune disorders."}],"volume":128,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","scopus_import":1,"publication":"Journal of Cell Science","_id":"477","issue":"15","author":[{"full_name":"Holst, Katrin","last_name":"Holst","first_name":"Katrin"},{"full_name":"Guseva, Daria","last_name":"Guseva","first_name":"Daria"},{"last_name":"Schindler","first_name":"Susann","full_name":"Schindler, Susann"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt","first_name":"Michael K"},{"full_name":"Braun, Armin","first_name":"Armin","last_name":"Braun"},{"full_name":"Chopra, Himpriya","last_name":"Chopra","first_name":"Himpriya"},{"last_name":"Pabst","first_name":"Oliver","full_name":"Pabst, Oliver"},{"full_name":"Ponimaskin, Evgeni","first_name":"Evgeni","last_name":"Ponimaskin"}],"department":[{"_id":"MiSi"}],"date_created":"2018-12-11T11:46:41Z","publication_status":"published","oa_version":"None","intvolume":"       128","month":"06","title":"The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells","quality_controlled":"1","page":"2866 - 2880","language":[{"iso":"eng"}],"publisher":"Company of Biologists"},{"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","volume":12,"type":"journal_article","date_published":"2015-09-25T00:00:00Z","citation":{"ista":"Bierbaum V, Klumpp S. 2015. Impact of the cell division cycle on gene circuits. Physical Biology. 12(6), 066003.","short":"V. Bierbaum, S. Klumpp, Physical Biology 12 (2015).","mla":"Bierbaum, Veronika, and Stefan Klumpp. “Impact of the Cell Division Cycle on Gene Circuits.” <i>Physical Biology</i>, vol. 12, no. 6, 066003, IOP Publishing Ltd., 2015, doi:<a href=\"https://doi.org/10.1088/1478-3975/12/6/066003\">10.1088/1478-3975/12/6/066003</a>.","chicago":"Bierbaum, Veronika, and Stefan Klumpp. “Impact of the Cell Division Cycle on Gene Circuits.” <i>Physical Biology</i>. IOP Publishing Ltd., 2015. <a href=\"https://doi.org/10.1088/1478-3975/12/6/066003\">https://doi.org/10.1088/1478-3975/12/6/066003</a>.","ieee":"V. Bierbaum and S. Klumpp, “Impact of the cell division cycle on gene circuits,” <i>Physical Biology</i>, vol. 12, no. 6. IOP Publishing Ltd., 2015.","apa":"Bierbaum, V., &#38; Klumpp, S. (2015). Impact of the cell division cycle on gene circuits. <i>Physical Biology</i>. IOP Publishing Ltd. <a href=\"https://doi.org/10.1088/1478-3975/12/6/066003\">https://doi.org/10.1088/1478-3975/12/6/066003</a>","ama":"Bierbaum V, Klumpp S. Impact of the cell division cycle on gene circuits. <i>Physical Biology</i>. 2015;12(6). doi:<a href=\"https://doi.org/10.1088/1478-3975/12/6/066003\">10.1088/1478-3975/12/6/066003</a>"},"year":"2015","date_updated":"2021-01-12T06:51:25Z","publist_id":"5641","abstract":[{"text":"In growing cells, protein synthesis and cell growth are typically not synchronous, and, thus, protein concentrations vary over the cell division cycle. We have developed a theoretical description of genetic regulatory systems in bacteria that explicitly considers the cell division cycle to investigate its impact on gene expression. We calculate the cell-to-cell variations arising from cells being at different stages in the division cycle for unregulated genes and for basic regulatory mechanisms. These variations contribute to the extrinsic noise observed in single-cell experiments, and are most significant for proteins with short lifetimes. Negative autoregulation buffers against variation of protein concentration over the division cycle, but the effect is found to be relatively weak. Stronger buffering is achieved by an increased protein lifetime. Positive autoregulation can strongly amplify such variation if the parameters are set to values that lead to resonance-like behaviour. For cooperative positive autoregulation, the concentration variation over the division cycle diminishes the parameter region of bistability and modulates the switching times between the two stable states. The same effects are seen for a two-gene mutual-repression toggle switch. By contrast, an oscillatory circuit, the repressilator, is only weakly affected by the division cycle.","lang":"eng"}],"day":"25","doi":"10.1088/1478-3975/12/6/066003","language":[{"iso":"eng"}],"quality_controlled":"1","publisher":"IOP Publishing Ltd.","issue":"6","author":[{"full_name":"Bierbaum, Veronika","first_name":"Veronika","last_name":"Bierbaum","id":"3FD04378-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Klumpp, Stefan","first_name":"Stefan","last_name":"Klumpp"}],"scopus_import":1,"_id":"1530","publication":"Physical Biology","intvolume":"        12","article_number":"066003","month":"09","title":"Impact of the cell division cycle on gene circuits","department":[{"_id":"MiSi"}],"date_created":"2018-12-11T11:52:33Z","publication_status":"published","oa_version":"None"},{"citation":{"ama":"Ruprecht V, Wieser S, Callan Jones A, et al. Cortical contractility triggers a stochastic switch to fast amoeboid cell motility. <i>Cell</i>. 2015;160(4):673-685. doi:<a href=\"https://doi.org/10.1016/j.cell.2015.01.008\">10.1016/j.cell.2015.01.008</a>","apa":"Ruprecht, V., Wieser, S., Callan Jones, A., Smutny, M., Morita, H., Sako, K., … Heisenberg, C.-P. J. (2015). Cortical contractility triggers a stochastic switch to fast amoeboid cell motility. <i>Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.cell.2015.01.008\">https://doi.org/10.1016/j.cell.2015.01.008</a>","chicago":"Ruprecht, Verena, Stefan Wieser, Andrew Callan Jones, Michael Smutny, Hitoshi Morita, Keisuke Sako, Vanessa Barone, et al. “Cortical Contractility Triggers a Stochastic Switch to Fast Amoeboid Cell Motility.” <i>Cell</i>. Cell Press, 2015. <a href=\"https://doi.org/10.1016/j.cell.2015.01.008\">https://doi.org/10.1016/j.cell.2015.01.008</a>.","ieee":"V. Ruprecht <i>et al.</i>, “Cortical contractility triggers a stochastic switch to fast amoeboid cell motility,” <i>Cell</i>, vol. 160, no. 4. Cell Press, pp. 673–685, 2015.","short":"V. Ruprecht, S. Wieser, A. Callan Jones, M. Smutny, H. Morita, K. Sako, V. Barone, M. Ritsch Marte, M.K. Sixt, R. Voituriez, C.-P.J. Heisenberg, Cell 160 (2015) 673–685.","mla":"Ruprecht, Verena, et al. “Cortical Contractility Triggers a Stochastic Switch to Fast Amoeboid Cell Motility.” <i>Cell</i>, vol. 160, no. 4, Cell Press, 2015, pp. 673–85, doi:<a href=\"https://doi.org/10.1016/j.cell.2015.01.008\">10.1016/j.cell.2015.01.008</a>.","ista":"Ruprecht V, Wieser S, Callan Jones A, Smutny M, Morita H, Sako K, Barone V, Ritsch Marte M, Sixt MK, Voituriez R, Heisenberg C-PJ. 2015. Cortical contractility triggers a stochastic switch to fast amoeboid cell motility. Cell. 160(4), 673–685."},"year":"2015","date_updated":"2023-09-07T12:05:08Z","abstract":[{"lang":"eng","text":"3D amoeboid cell migration is central to many developmental and disease-related processes such as cancer metastasis. Here, we identify a unique prototypic amoeboid cell migration mode in early zebrafish embryos, termed stable-bleb migration. Stable-bleb cells display an invariant polarized balloon-like shape with exceptional migration speed and persistence. Progenitor cells can be reversibly transformed into stable-bleb cells irrespective of their primary fate and motile characteristics by increasing myosin II activity through biochemical or mechanical stimuli. Using a combination of theory and experiments, we show that, in stable-bleb cells, cortical contractility fluctuations trigger a stochastic switch into amoeboid motility, and a positive feedback between cortical flows and gradients in contractility maintains stable-bleb cell polarization. We further show that rearward cortical flows drive stable-bleb cell migration in various adhesive and non-adhesive environments, unraveling a highly versatile amoeboid migration phenotype."}],"day":"12","doi":"10.1016/j.cell.2015.01.008","ddc":["570"],"acknowledgement":"We would like to thank R. Hausschild and E. Papusheva for technical assistance and the service facilities at the IST Austria for continuous support. The caRhoA plasmid was a kind gift of T. Kudoh and A. Takesono. We thank M. Piel and E. Paluch for exchanging unpublished data. ","volume":160,"issue":"4","author":[{"id":"4D71A03A-F248-11E8-B48F-1D18A9856A87","first_name":"Verena","last_name":"Ruprecht","orcid":"0000-0003-4088-8633","full_name":"Ruprecht, Verena"},{"id":"355AA5A0-F248-11E8-B48F-1D18A9856A87","last_name":"Wieser","first_name":"Stefan","full_name":"Wieser, Stefan","orcid":"0000-0002-2670-2217"},{"last_name":"Callan Jones","first_name":"Andrew","full_name":"Callan Jones, Andrew"},{"last_name":"Smutny","first_name":"Michael","full_name":"Smutny, Michael","orcid":"0000-0002-5920-9090","id":"3FE6E4E8-F248-11E8-B48F-1D18A9856A87"},{"id":"4C6E54C6-F248-11E8-B48F-1D18A9856A87","last_name":"Morita","first_name":"Hitoshi","full_name":"Morita, Hitoshi"},{"id":"3BED66BE-F248-11E8-B48F-1D18A9856A87","first_name":"Keisuke","last_name":"Sako","orcid":"0000-0002-6453-8075","full_name":"Sako, Keisuke"},{"orcid":"0000-0003-2676-3367","full_name":"Barone, Vanessa","first_name":"Vanessa","last_name":"Barone","id":"419EECCC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Monika","last_name":"Ritsch Marte","full_name":"Ritsch Marte, Monika"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Voituriez, Raphaël","last_name":"Voituriez","first_name":"Raphaël"},{"full_name":"Heisenberg, Carl-Philipp J","orcid":"0000-0002-0912-4566","last_name":"Heisenberg","first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87"}],"scopus_import":1,"_id":"1537","intvolume":"       160","pubrep_id":"484","title":"Cortical contractility triggers a stochastic switch to fast amoeboid cell motility","date_created":"2018-12-11T11:52:35Z","department":[{"_id":"CaHe"},{"_id":"MiSi"}],"publication_status":"published","file_date_updated":"2020-07-14T12:45:01Z","quality_controlled":"1","page":"673 - 685","publisher":"Cell Press","type":"journal_article","date_published":"2015-02-12T00:00:00Z","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"publist_id":"5634","oa":1,"status":"public","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","related_material":{"record":[{"relation":"dissertation_contains","id":"961","status":"public"}]},"file":[{"creator":"system","file_id":"5003","relation":"main_file","access_level":"open_access","file_name":"IST-2016-484-v1+1_1-s2.0-S0092867415000094-main.pdf","content_type":"application/pdf","date_updated":"2020-07-14T12:45:01Z","file_size":4362653,"checksum":"228d3edf40627d897b3875088a0ac51f","date_created":"2018-12-12T10:13:21Z"}],"has_accepted_license":"1","publication":"Cell","month":"02","project":[{"_id":"2529486C-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation","grant_number":"T 560-B17"},{"call_identifier":"FWF","_id":"2527D5CC-B435-11E9-9278-68D0E5697425","grant_number":"I 812-B12","name":"Cell Cortex and Germ Layer Formation in Zebrafish Gastrulation"}],"acknowledged_ssus":[{"_id":"SSU"}],"oa_version":"Published Version","language":[{"iso":"eng"}]},{"date_updated":"2021-01-12T06:51:33Z","year":"2015","citation":{"ieee":"P. Maiuri <i>et al.</i>, “Actin flows mediate a universal coupling between cell speed and cell persistence,” <i>Cell</i>, vol. 161, no. 2. Cell Press, pp. 374–386, 2015.","chicago":"Maiuri, Paolo, Jean Rupprecht, Stefan Wieser, Verena Ruprecht, Olivier Bénichou, Nicolas Carpi, Mathieu Coppey, et al. “Actin Flows Mediate a Universal Coupling between Cell Speed and Cell Persistence.” <i>Cell</i>. Cell Press, 2015. <a href=\"https://doi.org/10.1016/j.cell.2015.01.056\">https://doi.org/10.1016/j.cell.2015.01.056</a>.","ama":"Maiuri P, Rupprecht J, Wieser S, et al. Actin flows mediate a universal coupling between cell speed and cell persistence. <i>Cell</i>. 2015;161(2):374-386. doi:<a href=\"https://doi.org/10.1016/j.cell.2015.01.056\">10.1016/j.cell.2015.01.056</a>","apa":"Maiuri, P., Rupprecht, J., Wieser, S., Ruprecht, V., Bénichou, O., Carpi, N., … Voituriez, R. (2015). Actin flows mediate a universal coupling between cell speed and cell persistence. <i>Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.cell.2015.01.056\">https://doi.org/10.1016/j.cell.2015.01.056</a>","ista":"Maiuri P, Rupprecht J, Wieser S, Ruprecht V, Bénichou O, Carpi N, Coppey M, De Beco S, Gov N, Heisenberg C-PJ, Lage Crespo C, Lautenschlaeger F, Le Berre M, Lennon Duménil A, Raab M, Thiam H, Piel M, Sixt MK, Voituriez R. 2015. Actin flows mediate a universal coupling between cell speed and cell persistence. Cell. 161(2), 374–386.","mla":"Maiuri, Paolo, et al. “Actin Flows Mediate a Universal Coupling between Cell Speed and Cell Persistence.” <i>Cell</i>, vol. 161, no. 2, Cell Press, 2015, pp. 374–86, doi:<a href=\"https://doi.org/10.1016/j.cell.2015.01.056\">10.1016/j.cell.2015.01.056</a>.","short":"P. Maiuri, J. Rupprecht, S. Wieser, V. Ruprecht, O. Bénichou, N. Carpi, M. Coppey, S. De Beco, N. Gov, C.-P.J. Heisenberg, C. Lage Crespo, F. Lautenschlaeger, M. Le Berre, A. Lennon Duménil, M. Raab, H. Thiam, M. Piel, M.K. Sixt, R. Voituriez, Cell 161 (2015) 374–386."},"date_published":"2015-04-09T00:00:00Z","type":"journal_article","doi":"10.1016/j.cell.2015.01.056","day":"09","abstract":[{"text":"Cell movement has essential functions in development, immunity, and cancer. Various cell migration patterns have been reported, but no general rule has emerged so far. Here, we show on the basis of experimental data in vitro and in vivo that cell persistence, which quantifies the straightness of trajectories, is robustly coupled to cell migration speed. We suggest that this universal coupling constitutes a generic law of cell migration, which originates in the advection of polarity cues by an actin cytoskeleton undergoing flows at the cellular scale. Our analysis relies on a theoretical model that we validate by measuring the persistence of cells upon modulation of actin flow speeds and upon optogenetic manipulation of the binding of an actin regulator to actin filaments. Beyond the quantitative prediction of the coupling, the model yields a generic phase diagram of cellular trajectories, which recapitulates the full range of observed migration patterns.","lang":"eng"}],"publist_id":"5618","volume":161,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","publication":"Cell","_id":"1553","scopus_import":1,"author":[{"first_name":"Paolo","last_name":"Maiuri","full_name":"Maiuri, Paolo"},{"first_name":"Jean","last_name":"Rupprecht","full_name":"Rupprecht, Jean"},{"first_name":"Stefan","last_name":"Wieser","orcid":"0000-0002-2670-2217","full_name":"Wieser, Stefan","id":"355AA5A0-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Ruprecht, Verena","orcid":"0000-0003-4088-8633","last_name":"Ruprecht","first_name":"Verena","id":"4D71A03A-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Olivier","last_name":"Bénichou","full_name":"Bénichou, Olivier"},{"full_name":"Carpi, Nicolas","last_name":"Carpi","first_name":"Nicolas"},{"last_name":"Coppey","first_name":"Mathieu","full_name":"Coppey, Mathieu"},{"full_name":"De Beco, Simon","first_name":"Simon","last_name":"De Beco"},{"first_name":"Nir","last_name":"Gov","full_name":"Gov, Nir"},{"id":"39427864-F248-11E8-B48F-1D18A9856A87","first_name":"Carl-Philipp J","last_name":"Heisenberg","orcid":"0000-0002-0912-4566","full_name":"Heisenberg, Carl-Philipp J"},{"first_name":"Carolina","last_name":"Lage Crespo","full_name":"Lage Crespo, Carolina"},{"full_name":"Lautenschlaeger, Franziska","last_name":"Lautenschlaeger","first_name":"Franziska"},{"full_name":"Le Berre, Maël","last_name":"Le Berre","first_name":"Maël"},{"full_name":"Lennon Duménil, Ana","first_name":"Ana","last_name":"Lennon Duménil"},{"full_name":"Raab, Matthew","last_name":"Raab","first_name":"Matthew"},{"full_name":"Thiam, Hawa","first_name":"Hawa","last_name":"Thiam"},{"last_name":"Piel","first_name":"Matthieu","full_name":"Piel, Matthieu"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179"},{"full_name":"Voituriez, Raphaël","first_name":"Raphaël","last_name":"Voituriez"}],"issue":"2","oa_version":"None","publication_status":"published","date_created":"2018-12-11T11:52:41Z","department":[{"_id":"MiSi"},{"_id":"CaHe"}],"project":[{"call_identifier":"FWF","_id":"2529486C-B435-11E9-9278-68D0E5697425","grant_number":"T 560-B17","name":"Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation"},{"name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556","call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425"},{"_id":"25ABD200-B435-11E9-9278-68D0E5697425","grant_number":"RGP0058/2011","name":"Cell migration in complex environments: from in vivo experiments to theoretical models"}],"title":"Actin flows mediate a universal coupling between cell speed and cell persistence","month":"04","intvolume":"       161","page":"374 - 386","ec_funded":1,"quality_controlled":"1","language":[{"iso":"eng"}],"publisher":"Cell Press"},{"page":"338 - 340","quality_controlled":"1","language":[{"iso":"eng"}],"publisher":"Nature Publishing Group","_id":"1560","publication":"Nature Immunology","scopus_import":1,"author":[{"first_name":"Miroslav","last_name":"Hons","orcid":"0000-0002-6625-3348","full_name":"Hons, Miroslav","id":"4167FE56-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Sixt","first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"issue":"4","oa_version":"None","publication_status":"published","department":[{"_id":"MiSi"}],"date_created":"2018-12-11T11:52:43Z","title":"The lymph node filter revealed","month":"03","intvolume":"        16","volume":16,"status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2021-01-12T06:51:36Z","citation":{"chicago":"Hons, Miroslav, and Michael K Sixt. “The Lymph Node Filter Revealed.” <i>Nature Immunology</i>. Nature Publishing Group, 2015. <a href=\"https://doi.org/10.1038/ni.3126\">https://doi.org/10.1038/ni.3126</a>.","ieee":"M. Hons and M. K. Sixt, “The lymph node filter revealed,” <i>Nature Immunology</i>, vol. 16, no. 4. Nature Publishing Group, pp. 338–340, 2015.","ama":"Hons M, Sixt MK. The lymph node filter revealed. <i>Nature Immunology</i>. 2015;16(4):338-340. doi:<a href=\"https://doi.org/10.1038/ni.3126\">10.1038/ni.3126</a>","apa":"Hons, M., &#38; Sixt, M. K. (2015). The lymph node filter revealed. <i>Nature Immunology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/ni.3126\">https://doi.org/10.1038/ni.3126</a>","ista":"Hons M, Sixt MK. 2015. The lymph node filter revealed. Nature Immunology. 16(4), 338–340.","mla":"Hons, Miroslav, and Michael K. Sixt. “The Lymph Node Filter Revealed.” <i>Nature Immunology</i>, vol. 16, no. 4, Nature Publishing Group, 2015, pp. 338–40, doi:<a href=\"https://doi.org/10.1038/ni.3126\">10.1038/ni.3126</a>.","short":"M. Hons, M.K. Sixt, Nature Immunology 16 (2015) 338–340."},"year":"2015","date_published":"2015-03-19T00:00:00Z","type":"journal_article","doi":"10.1038/ni.3126","day":"19","abstract":[{"lang":"eng","text":"Stromal cells in the subcapsular sinus of the lymph node 'decide' which cells and molecules are allowed access to the deeper parenchyma. The glycoprotein PLVAP is a crucial component of this selector function."}],"publist_id":"5611"},{"scopus_import":1,"publication":"European Journal of Immunology","_id":"1561","issue":"6","author":[{"first_name":"Klaus","last_name":"Heger","full_name":"Heger, Klaus"},{"full_name":"Kober, Maike","first_name":"Maike","last_name":"Kober"},{"full_name":"Rieß, David","last_name":"Rieß","first_name":"David"},{"first_name":"Christoph","last_name":"Drees","full_name":"Drees, Christoph"},{"first_name":"Ingrid","last_name":"De Vries","full_name":"De Vries, Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Bertossi, Arianna","first_name":"Arianna","last_name":"Bertossi"},{"last_name":"Roers","first_name":"Axel","full_name":"Roers, Axel"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Marc","last_name":"Schmidt Supprian","full_name":"Schmidt Supprian, Marc"}],"department":[{"_id":"MiSi"}],"date_created":"2018-12-11T11:52:44Z","oa_version":"None","publication_status":"published","intvolume":"        45","title":"A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors","month":"06","quality_controlled":"1","page":"1614 - 1620","language":[{"iso":"eng"}],"publisher":"Wiley","year":"2015","citation":{"ista":"Heger K, Kober M, Rieß D, Drees C, de Vries I, Bertossi A, Roers A, Sixt MK, Schmidt Supprian M. 2015. A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors. European Journal of Immunology. 45(6), 1614–1620.","mla":"Heger, Klaus, et al. “A Novel Cre Recombinase Reporter Mouse Strain Facilitates Selective and Efficient Infection of Primary Immune Cells with Adenoviral Vectors.” <i>European Journal of Immunology</i>, vol. 45, no. 6, Wiley, 2015, pp. 1614–20, doi:<a href=\"https://doi.org/10.1002/eji.201545457\">10.1002/eji.201545457</a>.","short":"K. Heger, M. Kober, D. Rieß, C. Drees, I. de Vries, A. Bertossi, A. Roers, M.K. Sixt, M. Schmidt Supprian, European Journal of Immunology 45 (2015) 1614–1620.","chicago":"Heger, Klaus, Maike Kober, David Rieß, Christoph Drees, Ingrid de Vries, Arianna Bertossi, Axel Roers, Michael K Sixt, and Marc Schmidt Supprian. “A Novel Cre Recombinase Reporter Mouse Strain Facilitates Selective and Efficient Infection of Primary Immune Cells with Adenoviral Vectors.” <i>European Journal of Immunology</i>. Wiley, 2015. <a href=\"https://doi.org/10.1002/eji.201545457\">https://doi.org/10.1002/eji.201545457</a>.","ieee":"K. Heger <i>et al.</i>, “A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors,” <i>European Journal of Immunology</i>, vol. 45, no. 6. Wiley, pp. 1614–1620, 2015.","ama":"Heger K, Kober M, Rieß D, et al. A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors. <i>European Journal of Immunology</i>. 2015;45(6):1614-1620. doi:<a href=\"https://doi.org/10.1002/eji.201545457\">10.1002/eji.201545457</a>","apa":"Heger, K., Kober, M., Rieß, D., Drees, C., de Vries, I., Bertossi, A., … Schmidt Supprian, M. (2015). A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors. <i>European Journal of Immunology</i>. Wiley. <a href=\"https://doi.org/10.1002/eji.201545457\">https://doi.org/10.1002/eji.201545457</a>"},"date_updated":"2021-01-12T06:51:36Z","type":"journal_article","date_published":"2015-06-01T00:00:00Z","day":"01","doi":"10.1002/eji.201545457","publist_id":"5610","abstract":[{"lang":"eng","text":"Replication-deficient recombinant adenoviruses are potent vectors for the efficient transient expression of exogenous genes in resting immune cells. However, most leukocytes are refractory to efficient adenoviral transduction as they lack expression of the coxsackie/adenovirus receptor (CAR). To circumvent this obstacle, we generated the R26/CAG-CARΔ1StopF (where R26 is ROSA26 and CAG is CMV early enhancer/chicken β actin promoter) knock-in mouse line. This strain allows monitoring of in situ Cre recombinase activity through expression of CARΔ1. Simultaneously, CARΔ1 expression permits selective and highly efficient adenoviral transduction of immune cell populations, such as mast cells or T cells, directly ex vivo in bulk cultures without prior cell purification or activation. Furthermore, we show that CARΔ1 expression dramatically improves adenoviral infection of in vitro differentiated conventional and plasmacytoid dendritic cells (DCs), basophils, mast cells, as well as Hoxb8-immortalized hematopoietic progenitor cells. This novel dual function mouse strain will hence be a valuable tool to rapidly dissect the function of specific genes in leukocyte physiology."}],"volume":45,"status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87"}]