[{"scopus_import":1,"article_processing_charge":"Yes","has_accepted_license":"1","day":"02","page":"902 - 909","citation":{"ama":"Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 2017;19(5):902-909. doi:10.1016/j.celrep.2017.04.027","ista":"Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909.","ieee":"K. Vaahtomeri et al., “Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia,” Cell Reports, vol. 19, no. 5. Cell Press, pp. 902–909, 2017.","apa":"Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling, M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.027","mla":"Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports, vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:10.1016/j.celrep.2017.04.027.","short":"K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling, W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909.","chicago":"Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.027."},"publication":"Cell Reports","date_published":"2017-05-02T00:00:00Z","type":"journal_article","issue":"5","abstract":[{"lang":"eng","text":"Trafficking cells frequently transmigrate through epithelial and endothelial monolayers. How monolayers cooperate with the penetrating cells to support their transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic capillaries as a model system for transendothelial migration. We find that the chemokine CCL21, which is the decisive guidance cue for intravasation, mainly localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes extracellularly enriched at the sites of endothelial cell-cell junctions. When we reconstitute the transmigration process in vitro, we find that secretion of CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and selective calcium chelation in lymphatic endothelium attenuates transmigration. Altogether, our data demonstrate a chemokine-mediated feedback between DCs and lymphatic endothelium, which facilitates transendothelial migration."}],"intvolume":" 19","status":"public","ddc":["570"],"title":"Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","_id":"672","oa_version":"Published Version","file":[{"relation":"main_file","file_id":"5109","date_created":"2018-12-12T10:14:54Z","date_updated":"2020-07-14T12:47:38Z","checksum":"8fdddaab1f1d76a6ec9ca94dcb6b07a2","file_name":"IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf","access_level":"open_access","content_type":"application/pdf","file_size":2248814,"creator":"system"}],"pubrep_id":"900","publication_identifier":{"issn":["22111247"]},"month":"05","project":[{"_id":"25A603A2-B435-11E9-9278-68D0E5697425","grant_number":"281556","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","call_identifier":"FP7"},{"grant_number":"Y 564-B12","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","call_identifier":"FWF"}],"quality_controlled":"1","tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)","image":"/images/cc_by_nc_nd.png"},"oa":1,"language":[{"iso":"eng"}],"doi":"10.1016/j.celrep.2017.04.027","license":"https://creativecommons.org/licenses/by-nc-nd/4.0/","ec_funded":1,"publist_id":"7052","file_date_updated":"2020-07-14T12:47:38Z","department":[{"_id":"MiSi"},{"_id":"Bio"},{"_id":"EM-Fac"}],"publisher":"Cell Press","publication_status":"published","year":"2017","volume":19,"date_updated":"2023-02-23T12:50:09Z","date_created":"2018-12-11T11:47:50Z","author":[{"full_name":"Vaahtomeri, Kari","id":"368EE576-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7829-3518","first_name":"Kari","last_name":"Vaahtomeri"},{"id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","last_name":"Brown","first_name":"Markus","full_name":"Brown, Markus"},{"id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9843-3522","first_name":"Robert","last_name":"Hauschild","full_name":"Hauschild, Robert"},{"full_name":"De Vries, Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid","last_name":"De Vries"},{"full_name":"Leithner, Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander F","last_name":"Leithner"},{"full_name":"Mehling, Matthias","orcid":"0000-0001-8599-1226","id":"3C23B994-F248-11E8-B48F-1D18A9856A87","last_name":"Mehling","first_name":"Matthias"},{"first_name":"Walter","last_name":"Kaufmann","id":"3F99E422-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9735-5315","full_name":"Kaufmann, Walter"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","first_name":"Michael K","last_name":"Sixt","full_name":"Sixt, Michael K"}]},{"type":"journal_article","issue":"9","abstract":[{"text":"Navigation of cells along gradients of guidance cues is a determining step in many developmental and immunological processes. Gradients can either be soluble or immobilized to tissues as demonstrated for the haptotactic migration of dendritic cells (DCs) toward higher concentrations of immobilized chemokine CCL21. To elucidate how gradient characteristics govern cellular response patterns, we here introduce an in vitro system allowing to track migratory responses of DCs to precisely controlled immobilized gradients of CCL21. We find that haptotactic sensing depends on the absolute CCL21 concentration and local steepness of the gradient, consistent with a scenario where DC directionality is governed by the signal-to-noise ratio of CCL21 binding to the receptor CCR7. We find that the conditions for optimal DC guidance are perfectly provided by the CCL21 gradients we measure in vivo. Furthermore, we find that CCR7 signal termination by the G-protein-coupled receptor kinase 6 (GRK6) is crucial for haptotactic but dispensable for chemotactic CCL21 gradient sensing in vitro and confirm those observations in vivo. These findings suggest that stable, tissue-bound CCL21 gradients as sustainable “roads” ensure optimal guidance in vivo.","lang":"eng"}],"_id":"674","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","intvolume":" 27","title":"Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6","status":"public","oa_version":"None","scopus_import":1,"day":"09","citation":{"short":"J. Schwarz, V. Bierbaum, K. Vaahtomeri, R. Hauschild, M. Brown, I. de Vries, A.F. Leithner, A. Reversat, J. Merrin, T. Tarrant, M.T. Bollenbach, M.K. Sixt, Current Biology 27 (2017) 1314–1325.","mla":"Schwarz, Jan, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current Biology, vol. 27, no. 9, Cell Press, 2017, pp. 1314–25, doi:10.1016/j.cub.2017.04.004.","chicago":"Schwarz, Jan, Veronika Bierbaum, Kari Vaahtomeri, Robert Hauschild, Markus Brown, Ingrid de Vries, Alexander F Leithner, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2017.04.004.","ama":"Schwarz J, Bierbaum V, Vaahtomeri K, et al. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. 2017;27(9):1314-1325. doi:10.1016/j.cub.2017.04.004","ieee":"J. Schwarz et al., “Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6,” Current Biology, vol. 27, no. 9. Cell Press, pp. 1314–1325, 2017.","apa":"Schwarz, J., Bierbaum, V., Vaahtomeri, K., Hauschild, R., Brown, M., de Vries, I., … Sixt, M. K. (2017). Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2017.04.004","ista":"Schwarz J, Bierbaum V, Vaahtomeri K, Hauschild R, Brown M, de Vries I, Leithner AF, Reversat A, Merrin J, Tarrant T, Bollenbach MT, Sixt MK. 2017. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. 27(9), 1314–1325."},"publication":"Current Biology","page":"1314 - 1325","date_published":"2017-05-09T00:00:00Z","publist_id":"7050","ec_funded":1,"year":"2017","department":[{"_id":"MiSi"},{"_id":"Bio"},{"_id":"NanoFab"}],"publisher":"Cell Press","publication_status":"published","author":[{"last_name":"Schwarz","first_name":"Jan","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","full_name":"Schwarz, Jan"},{"full_name":"Bierbaum, Veronika","id":"3FD04378-F248-11E8-B48F-1D18A9856A87","last_name":"Bierbaum","first_name":"Veronika"},{"full_name":"Vaahtomeri, Kari","orcid":"0000-0001-7829-3518","id":"368EE576-F248-11E8-B48F-1D18A9856A87","last_name":"Vaahtomeri","first_name":"Kari"},{"full_name":"Hauschild, Robert","last_name":"Hauschild","first_name":"Robert","orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Markus","last_name":"Brown","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","full_name":"Brown, Markus"},{"full_name":"De Vries, Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","last_name":"De Vries","first_name":"Ingrid"},{"last_name":"Leithner","first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","full_name":"Leithner, Alexander F"},{"full_name":"Reversat, Anne","first_name":"Anne","last_name":"Reversat","id":"35B76592-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-0666-8928"},{"full_name":"Merrin, Jack","orcid":"0000-0001-5145-4609","id":"4515C308-F248-11E8-B48F-1D18A9856A87","last_name":"Merrin","first_name":"Jack"},{"full_name":"Tarrant, Teresa","first_name":"Teresa","last_name":"Tarrant"},{"last_name":"Bollenbach","first_name":"Tobias","orcid":"0000-0003-4398-476X","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","full_name":"Bollenbach, Tobias"},{"full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"volume":27,"date_updated":"2023-02-23T12:50:44Z","date_created":"2018-12-11T11:47:51Z","publication_identifier":{"issn":["09609822"]},"month":"05","project":[{"name":"International IST Postdoc Fellowship Programme","call_identifier":"FP7","_id":"25681D80-B435-11E9-9278-68D0E5697425","grant_number":"291734"},{"grant_number":"Y 564-B12","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)"}],"quality_controlled":"1","doi":"10.1016/j.cub.2017.04.004","language":[{"iso":"eng"}]},{"pubrep_id":"899","file":[{"file_name":"IST-2017-899-v1+1_1-s2.0-S2211124717305454-main.pdf","access_level":"open_access","creator":"system","file_size":3005610,"content_type":"application/pdf","file_id":"5171","relation":"main_file","date_updated":"2020-07-14T12:47:40Z","date_created":"2018-12-12T10:15:48Z","checksum":"efc7287d9c6354983cb151880e9ad72a"}],"oa_version":"Published Version","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"677","intvolume":" 19","ddc":["570"],"status":"public","title":"The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination","issue":"7","abstract":[{"lang":"eng","text":"The INO80 complex (INO80-C) is an evolutionarily conserved nucleosome remodeler that acts in transcription, replication, and genome stability. It is required for resistance against genotoxic agents and is involved in the repair of DNA double-strand breaks (DSBs) by homologous recombination (HR). However, the causes of the HR defect in INO80-C mutant cells are controversial. Here, we unite previous findings using a system to study HR with high spatial resolution in budding yeast. We find that INO80-C has at least two distinct functions during HR—DNA end resection and presynaptic filament formation. Importantly, the second function is linked to the histone variant H2A.Z. In the absence of H2A.Z, presynaptic filament formation and HR are restored in INO80-C-deficient mutants, suggesting that presynaptic filament formation is the crucial INO80-C function during HR."}],"type":"journal_article","date_published":"2017-05-16T00:00:00Z","citation":{"ista":"Lademann C, Renkawitz J, Pfander B, Jentsch S. 2017. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. 19(7), 1294–1303.","apa":"Lademann, C., Renkawitz, J., Pfander, B., & Jentsch, S. (2017). The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.051","ieee":"C. Lademann, J. Renkawitz, B. Pfander, and S. Jentsch, “The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination,” Cell Reports, vol. 19, no. 7. Cell Press, pp. 1294–1303, 2017.","ama":"Lademann C, Renkawitz J, Pfander B, Jentsch S. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. 2017;19(7):1294-1303. doi:10.1016/j.celrep.2017.04.051","chicago":"Lademann, Claudio, Jörg Renkawitz, Boris Pfander, and Stefan Jentsch. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.051.","mla":"Lademann, Claudio, et al. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” Cell Reports, vol. 19, no. 7, Cell Press, 2017, pp. 1294–303, doi:10.1016/j.celrep.2017.04.051.","short":"C. Lademann, J. Renkawitz, B. Pfander, S. Jentsch, Cell Reports 19 (2017) 1294–1303."},"publication":"Cell Reports","page":"1294 - 1303","has_accepted_license":"1","day":"16","scopus_import":1,"author":[{"last_name":"Lademann","first_name":"Claudio","full_name":"Lademann, Claudio"},{"id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2856-3369","first_name":"Jörg","last_name":"Renkawitz","full_name":"Renkawitz, Jörg"},{"full_name":"Pfander, Boris","first_name":"Boris","last_name":"Pfander"},{"first_name":"Stefan","last_name":"Jentsch","full_name":"Jentsch, Stefan"}],"volume":19,"date_updated":"2021-01-12T08:08:57Z","date_created":"2018-12-11T11:47:52Z","year":"2017","publisher":"Cell Press","department":[{"_id":"MiSi"}],"publication_status":"published","publist_id":"7046","file_date_updated":"2020-07-14T12:47:40Z","doi":"10.1016/j.celrep.2017.04.051","language":[{"iso":"eng"}],"tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)","image":"/images/cc_by_nc_nd.png"},"oa":1,"quality_controlled":"1","publication_identifier":{"issn":["22111247"]},"month":"05"},{"day":"01","has_accepted_license":"1","scopus_import":1,"date_published":"2017-07-01T00:00:00Z","publication":"Journal of Cell Science","citation":{"chicago":"Veß, Astrid, Ulrich Blache, Laura Leitner, Angela Kurz, Anja Ehrenpfordt, Michael K Sixt, and Guido Posern. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell Science. Company of Biologists, 2017. https://doi.org/10.1242/jcs.200899.","short":"A. Veß, U. Blache, L. Leitner, A. Kurz, A. Ehrenpfordt, M.K. Sixt, G. Posern, Journal of Cell Science 130 (2017) 2172–2184.","mla":"Veß, Astrid, et al. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell Science, vol. 130, no. 13, Company of Biologists, 2017, pp. 2172–84, doi:10.1242/jcs.200899.","apa":"Veß, A., Blache, U., Leitner, L., Kurz, A., Ehrenpfordt, A., Sixt, M. K., & Posern, G. (2017). A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.200899","ieee":"A. Veß et al., “A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity,” Journal of Cell Science, vol. 130, no. 13. Company of Biologists, pp. 2172–2184, 2017.","ista":"Veß A, Blache U, Leitner L, Kurz A, Ehrenpfordt A, Sixt MK, Posern G. 2017. A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. 130(13), 2172–2184.","ama":"Veß A, Blache U, Leitner L, et al. A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. 2017;130(13):2172-2184. doi:10.1242/jcs.200899"},"article_type":"original","page":"2172 - 2184","abstract":[{"lang":"eng","text":"A change regarding the extent of adhesion - hereafter referred to as adhesion plasticity - between adhesive and less-adhesive states of mammalian cells is important for their behavior. To investigate adhesion plasticity, we have selected a stable isogenic subpopulation of human MDA-MB-468 breast carcinoma cells growing in suspension. These suspension cells are unable to re-adhere to various matrices or to contract three-dimensional collagen lattices. By using transcriptome analysis, we identified the focal adhesion protein tensin3 (Tns3) as a determinant of adhesion plasticity. Tns3 is strongly reduced at mRNA and protein levels in suspension cells. Furthermore, by transiently challenging breast cancer cells to grow under non-adherent conditions markedly reduces Tns3 protein expression, which is regained upon re-adhesion. Stable knockdown of Tns3 in parental MDA-MB-468 cells results in defective adhesion, spreading and migration. Tns3-knockdown cells display impaired structure and dynamics of focal adhesion complexes as determined by immunostaining. Restoration of Tns3 protein expression in suspension cells partially rescues adhesion and focal contact composition. Our work identifies Tns3 as a crucial focal adhesion component regulated by, and functionally contributing to, the switch between adhesive and non-adhesive states in MDA-MB-468 cancer cells."}],"issue":"13","type":"journal_article","oa_version":"Published Version","file":[{"file_name":"2017_CellScience_Vess.pdf","access_level":"open_access","creator":"dernst","file_size":10847596,"content_type":"application/pdf","file_id":"6966","relation":"main_file","date_created":"2019-10-24T09:43:56Z","date_updated":"2020-07-14T12:47:45Z","checksum":"42c81a0a4fc3128883b391c3af3f74bc"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"694","status":"public","title":"A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity","ddc":["570"],"intvolume":" 130","month":"07","publication_identifier":{"issn":["00219533"]},"doi":"10.1242/jcs.200899","language":[{"iso":"eng"}],"oa":1,"external_id":{"pmid":["28515231"]},"quality_controlled":"1","file_date_updated":"2020-07-14T12:47:45Z","publist_id":"7008","author":[{"last_name":"Veß","first_name":"Astrid","full_name":"Veß, Astrid"},{"full_name":"Blache, Ulrich","last_name":"Blache","first_name":"Ulrich"},{"first_name":"Laura","last_name":"Leitner","full_name":"Leitner, Laura"},{"first_name":"Angela","last_name":"Kurz","full_name":"Kurz, Angela"},{"last_name":"Ehrenpfordt","first_name":"Anja","full_name":"Ehrenpfordt, Anja"},{"first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"},{"full_name":"Posern, Guido","last_name":"Posern","first_name":"Guido"}],"date_created":"2018-12-11T11:47:58Z","date_updated":"2021-01-12T08:09:41Z","volume":130,"year":"2017","pmid":1,"publication_status":"published","publisher":"Company of Biologists","department":[{"_id":"MiSi"}]},{"publication_identifier":{"issn":["09609822"]},"month":"01","quality_controlled":"1","isi":1,"external_id":{"isi":["000391902500010"]},"language":[{"iso":"eng"}],"doi":"10.1016/j.cub.2016.11.035","publist_id":"6197","publisher":"Cell Press","department":[{"_id":"MiSi"}],"publication_status":"published","year":"2017","volume":27,"date_created":"2018-12-11T11:50:29Z","date_updated":"2023-09-20T11:28:19Z","author":[{"full_name":"Müller, Jan","last_name":"Müller","first_name":"Jan","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D"},{"full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"}],"scopus_import":"1","article_processing_charge":"No","day":"09","page":"R24 - R25","citation":{"short":"J. Müller, M.K. Sixt, Current Biology 27 (2017) R24–R25.","mla":"Müller, Jan, and Michael K. Sixt. “Cell Migration: Making the Waves.” Current Biology, vol. 27, no. 1, Cell Press, 2017, pp. R24–25, doi:10.1016/j.cub.2016.11.035.","chicago":"Müller, Jan, and Michael K Sixt. “Cell Migration: Making the Waves.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2016.11.035.","ama":"Müller J, Sixt MK. Cell migration: Making the waves. Current Biology. 2017;27(1):R24-R25. doi:10.1016/j.cub.2016.11.035","apa":"Müller, J., & Sixt, M. K. (2017). Cell migration: Making the waves. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2016.11.035","ieee":"J. Müller and M. K. Sixt, “Cell migration: Making the waves,” Current Biology, vol. 27, no. 1. Cell Press, pp. R24–R25, 2017.","ista":"Müller J, Sixt MK. 2017. Cell migration: Making the waves. Current Biology. 27(1), R24–R25."},"publication":"Current Biology","date_published":"2017-01-09T00:00:00Z","type":"journal_article","issue":"1","abstract":[{"text":"Coordinated changes of cell shape are often the result of the excitable, wave-like dynamics of the actin cytoskeleton. New work shows that, in migrating cells, protrusion waves arise from mechanochemical crosstalk between adhesion sites, membrane tension and the actin protrusive machinery.","lang":"eng"}],"intvolume":" 27","status":"public","title":"Cell migration: Making the waves","_id":"1161","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","oa_version":"None"},{"ec_funded":1,"publist_id":"6951","date_updated":"2023-09-28T11:33:49Z","date_created":"2018-12-11T11:48:10Z","volume":171,"author":[{"full_name":"Mueller, Jan","last_name":"Mueller","first_name":"Jan"},{"full_name":"Szep, Gregory","id":"4BFB7762-F248-11E8-B48F-1D18A9856A87","first_name":"Gregory","last_name":"Szep"},{"full_name":"Nemethova, Maria","id":"34E27F1C-F248-11E8-B48F-1D18A9856A87","first_name":"Maria","last_name":"Nemethova"},{"id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","last_name":"De Vries","first_name":"Ingrid","full_name":"De Vries, Ingrid"},{"full_name":"Lieber, Arnon","first_name":"Arnon","last_name":"Lieber"},{"full_name":"Winkler, Christoph","first_name":"Christoph","last_name":"Winkler"},{"first_name":"Karsten","last_name":"Kruse","full_name":"Kruse, Karsten"},{"last_name":"Small","first_name":"John","full_name":"Small, John"},{"full_name":"Schmeiser, Christian","last_name":"Schmeiser","first_name":"Christian"},{"first_name":"Kinneret","last_name":"Keren","full_name":"Keren, Kinneret"},{"full_name":"Hauschild, Robert","orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","last_name":"Hauschild","first_name":"Robert"},{"full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"publication_status":"published","department":[{"_id":"MiSi"},{"_id":"Bio"}],"publisher":"Cell Press","year":"2017","month":"09","publication_identifier":{"issn":["00928674"]},"acknowledged_ssus":[{"_id":"ScienComp"}],"language":[{"iso":"eng"}],"doi":"10.1016/j.cell.2017.07.051","isi":1,"quality_controlled":"1","project":[{"_id":"25AD6156-B435-11E9-9278-68D0E5697425","grant_number":"LS13-029","name":"Modeling of Polarization and Motility of Leukocytes in Three-Dimensional Environments"},{"call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","_id":"25A603A2-B435-11E9-9278-68D0E5697425","grant_number":"281556"}],"external_id":{"isi":["000411331800020"]},"abstract":[{"lang":"eng","text":"Actin filaments polymerizing against membranes power endocytosis, vesicular traffic, and cell motility. In vitro reconstitution studies suggest that the structure and the dynamics of actin networks respond to mechanical forces. We demonstrate that lamellipodial actin of migrating cells responds to mechanical load when membrane tension is modulated. In a steady state, migrating cell filaments assume the canonical dendritic geometry, defined by Arp2/3-generated 70° branch points. Increased tension triggers a dense network with a broadened range of angles, whereas decreased tension causes a shift to a sparse configuration dominated by filaments growing perpendicularly to the plasma membrane. We show that these responses emerge from the geometry of branched actin: when load per filament decreases, elongation speed increases and perpendicular filaments gradually outcompete others because they polymerize the shortest distance to the membrane, where they are protected from capping. This network-intrinsic geometrical adaptation mechanism tunes protrusive force in response to mechanical load."}],"issue":"1","type":"journal_article","oa_version":"None","status":"public","title":"Load adaptation of lamellipodial actin networks","intvolume":" 171","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","_id":"727","day":"21","article_processing_charge":"No","scopus_import":"1","date_published":"2017-09-21T00:00:00Z","page":"188 - 200","publication":"Cell","citation":{"ieee":"J. Mueller et al., “Load adaptation of lamellipodial actin networks,” Cell, vol. 171, no. 1. Cell Press, pp. 188–200, 2017.","apa":"Mueller, J., Szep, G., Nemethova, M., de Vries, I., Lieber, A., Winkler, C., … Sixt, M. K. (2017). Load adaptation of lamellipodial actin networks. Cell. Cell Press. https://doi.org/10.1016/j.cell.2017.07.051","ista":"Mueller J, Szep G, Nemethova M, de Vries I, Lieber A, Winkler C, Kruse K, Small J, Schmeiser C, Keren K, Hauschild R, Sixt MK. 2017. Load adaptation of lamellipodial actin networks. Cell. 171(1), 188–200.","ama":"Mueller J, Szep G, Nemethova M, et al. Load adaptation of lamellipodial actin networks. Cell. 2017;171(1):188-200. doi:10.1016/j.cell.2017.07.051","chicago":"Mueller, Jan, Gregory Szep, Maria Nemethova, Ingrid de Vries, Arnon Lieber, Christoph Winkler, Karsten Kruse, et al. “Load Adaptation of Lamellipodial Actin Networks.” Cell. Cell Press, 2017. https://doi.org/10.1016/j.cell.2017.07.051.","short":"J. Mueller, G. Szep, M. Nemethova, I. de Vries, A. Lieber, C. Winkler, K. Kruse, J. Small, C. Schmeiser, K. Keren, R. Hauschild, M.K. Sixt, Cell 171 (2017) 188–200.","mla":"Mueller, Jan, et al. “Load Adaptation of Lamellipodial Actin Networks.” Cell, vol. 171, no. 1, Cell Press, 2017, pp. 188–200, doi:10.1016/j.cell.2017.07.051."}},{"has_accepted_license":"1","article_processing_charge":"No","month":"08","day":"09","keyword":["Immunological synapse"],"date_published":"2017-08-09T00:00:00Z","doi":"10.15479/AT:ISTA:71","tmp":{"short":"CC0 (1.0)","image":"/images/cc_0.png","legal_code_url":"https://creativecommons.org/publicdomain/zero/1.0/legalcode","name":"Creative Commons Public Domain Dedication (CC0 1.0)"},"citation":{"chicago":"Leithner, Alexander F. “Immunological Synapse DC-Tcells.” Institute of Science and Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:71.","mla":"Leithner, Alexander F. Immunological Synapse DC-Tcells. Institute of Science and Technology Austria, 2017, doi:10.15479/AT:ISTA:71.","short":"A.F. Leithner, (2017).","ista":"Leithner AF. 2017. Immunological synapse DC-Tcells, Institute of Science and Technology Austria, 10.15479/AT:ISTA:71.","apa":"Leithner, A. F. (2017). Immunological synapse DC-Tcells. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:71","ieee":"A. F. Leithner, “Immunological synapse DC-Tcells.” Institute of Science and Technology Austria, 2017.","ama":"Leithner AF. Immunological synapse DC-Tcells. 2017. doi:10.15479/AT:ISTA:71"},"oa":1,"abstract":[{"text":"Immunological synapse DC-Tcells","lang":"eng"}],"file_date_updated":"2020-07-14T12:47:04Z","license":"https://creativecommons.org/publicdomain/zero/1.0/","type":"research_data","datarep_id":"71","author":[{"last_name":"Leithner","first_name":"Alexander F","orcid":"0000-0002-1073-744X","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","full_name":"Leithner, Alexander F"}],"oa_version":"Published Version","file":[{"relation":"main_file","file_id":"5612","date_created":"2018-12-12T13:02:47Z","date_updated":"2020-07-14T12:47:04Z","checksum":"3d6942d47d0737d064706b5728c4d8c8","file_name":"IST-2017-71-v1+1_Synapse_1.avi","access_level":"open_access","content_type":"video/x-msvideo","file_size":236204020,"creator":"system"},{"file_id":"5613","relation":"main_file","date_updated":"2020-07-14T12:47:04Z","date_created":"2018-12-12T13:02:51Z","checksum":"4850006c047b0147a9e85b3c2f6f0af4","file_name":"IST-2017-71-v1+2_Synapse_2.avi","access_level":"open_access","creator":"system","content_type":"video/x-msvideo","file_size":226232496}],"date_created":"2018-12-12T12:31:34Z","date_updated":"2024-02-21T13:47:00Z","_id":"5567","year":"2017","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","department":[{"_id":"MiSi"}],"publisher":"Institute of Science and Technology Austria","status":"public","title":"Immunological synapse DC-Tcells","ddc":["570"]},{"month":"04","day":"18","publication_identifier":{"issn":["10747613"]},"scopus_import":1,"language":[{"iso":"eng"}],"date_published":"2017-04-18T00:00:00Z","doi":"10.1016/j.immuni.2017.04.006","quality_controlled":"1","page":"519 - 520","publication":"Immunity","citation":{"short":"F.P. Assen, M.K. Sixt, Immunity 46 (2017) 519–520.","mla":"Assen, Frank P., and Michael K. Sixt. “The Dynamic Cytokine Niche.” Immunity, vol. 46, no. 4, Cell Press, 2017, pp. 519–20, doi:10.1016/j.immuni.2017.04.006.","chicago":"Assen, Frank P, and Michael K Sixt. “The Dynamic Cytokine Niche.” Immunity. Cell Press, 2017. https://doi.org/10.1016/j.immuni.2017.04.006.","ama":"Assen FP, Sixt MK. The dynamic cytokine niche. Immunity. 2017;46(4):519-520. doi:10.1016/j.immuni.2017.04.006","ieee":"F. P. Assen and M. K. Sixt, “The dynamic cytokine niche,” Immunity, vol. 46, no. 4. Cell Press, pp. 519–520, 2017.","apa":"Assen, F. P., & Sixt, M. K. (2017). The dynamic cytokine niche. Immunity. Cell Press. https://doi.org/10.1016/j.immuni.2017.04.006","ista":"Assen FP, Sixt MK. 2017. The dynamic cytokine niche. Immunity. 46(4), 519–520."},"abstract":[{"text":"Immune cells communicate using cytokine signals, but the quantitative rules of this communication aren't clear. In this issue of Immunity, Oyler-Yaniv et al. (2017) suggest that the distribution of a cytokine within a lymphatic organ is primarily governed by the local density of cells consuming it.","lang":"eng"}],"issue":"4","publist_id":"7065","type":"journal_article","date_created":"2018-12-11T11:47:47Z","date_updated":"2024-03-28T23:30:09Z","oa_version":"None","volume":46,"author":[{"first_name":"Frank P","last_name":"Assen","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-3470-6119","full_name":"Assen, Frank P"},{"first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"}],"related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"6947"}]},"publication_status":"published","status":"public","title":"The dynamic cytokine niche","intvolume":" 46","publisher":"Cell Press","department":[{"_id":"MiSi"}],"_id":"664","year":"2017","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87"},{"type":"journal_article","abstract":[{"lang":"eng","text":"Protective responses against pathogens require a rapid mobilization of resting neutrophils and the timely removal of activated ones. Neutrophils are exceptionally short-lived leukocytes, yet it remains unclear whether the lifespan of pathogen-engaged neutrophils is regulated differently from that in the circulating steady-state pool. Here, we have found that under homeostatic conditions, the mRNA-destabilizing protein tristetraprolin (TTP) regulates apoptosis and the numbers of activated infiltrating murine neutrophils but not neutrophil cellularity. Activated TTP-deficient neutrophils exhibited decreased apoptosis and enhanced accumulation at the infection site. In the context of myeloid-specific deletion of Ttp, the potentiation of neutrophil deployment protected mice against lethal soft tissue infection with Streptococcus pyogenes and prevented bacterial dissemination. Neutrophil transcriptome analysis revealed that decreased apoptosis of TTP-deficient neutrophils was specifically associated with elevated expression of myeloid cell leukemia 1 (Mcl1) but not other antiapoptotic B cell leukemia/ lymphoma 2 (Bcl2) family members. Higher Mcl1 expression resulted from stabilization of Mcl1 mRNA in the absence of TTP. The low apoptosis rate of infiltrating TTP-deficient neutrophils was comparable to that of transgenic Mcl1-overexpressing neutrophils. Our study demonstrates that posttranscriptional gene regulation by TTP schedules the termination of the antimicrobial engagement of neutrophils. The balancing role of TTP comes at the cost of an increased risk of bacterial infections."}],"issue":"6","status":"public","title":"The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection","intvolume":" 127","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"679","oa_version":"Submitted Version","scopus_import":1,"day":"01","page":"2051 - 2065","publication":"The Journal of Clinical Investigation","citation":{"short":"F. Ebner, V. Sedlyarov, S. Tasciyan, M. Ivin, F. Kratochvill, N. Gratz, L. Kenner, A. Villunger, M.K. Sixt, P. Kovarik, The Journal of Clinical Investigation 127 (2017) 2051–2065.","mla":"Ebner, Florian, et al. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged Neutrophils during Bacterial Infection.” The Journal of Clinical Investigation, vol. 127, no. 6, American Society for Clinical Investigation, 2017, pp. 2051–65, doi:10.1172/JCI80631.","chicago":"Ebner, Florian, Vitaly Sedlyarov, Saren Tasciyan, Masa Ivin, Franz Kratochvill, Nina Gratz, Lukas Kenner, Andreas Villunger, Michael K Sixt, and Pavel Kovarik. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged Neutrophils during Bacterial Infection.” The Journal of Clinical Investigation. American Society for Clinical Investigation, 2017. https://doi.org/10.1172/JCI80631.","ama":"Ebner F, Sedlyarov V, Tasciyan S, et al. The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. 2017;127(6):2051-2065. doi:10.1172/JCI80631","ieee":"F. Ebner et al., “The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection,” The Journal of Clinical Investigation, vol. 127, no. 6. American Society for Clinical Investigation, pp. 2051–2065, 2017.","apa":"Ebner, F., Sedlyarov, V., Tasciyan, S., Ivin, M., Kratochvill, F., Gratz, N., … Kovarik, P. (2017). The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. American Society for Clinical Investigation. https://doi.org/10.1172/JCI80631","ista":"Ebner F, Sedlyarov V, Tasciyan S, Ivin M, Kratochvill F, Gratz N, Kenner L, Villunger A, Sixt MK, Kovarik P. 2017. The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. 127(6), 2051–2065."},"date_published":"2017-06-01T00:00:00Z","publist_id":"7038","publication_status":"published","publisher":"American Society for Clinical Investigation","department":[{"_id":"MiSi"}],"year":"2017","acknowledgement":"This work was supported by grants from the Austrian Science Fund (FWF) (P27538-B21, I1621-B22, and SFB 43, to PK); by funding from the European Union Seventh Framework Programme Marie Curie Initial Training Networks (FP7-PEOPLE-2012-ITN) for the project INBIONET (INfection BIOlogy Training NETwork under grant agreement PITN-GA-2012-316682; and by a joint research cluster initiative of the University of Vienna and the Medical University of Vienna.","pmid":1,"date_updated":"2024-03-28T23:30:23Z","date_created":"2018-12-11T11:47:53Z","volume":127,"author":[{"first_name":"Florian","last_name":"Ebner","full_name":"Ebner, Florian"},{"full_name":"Sedlyarov, Vitaly","first_name":"Vitaly","last_name":"Sedlyarov"},{"orcid":"0000-0003-1671-393X","id":"4323B49C-F248-11E8-B48F-1D18A9856A87","last_name":"Tasciyan","first_name":"Saren","full_name":"Tasciyan, Saren"},{"full_name":"Ivin, Masa","last_name":"Ivin","first_name":"Masa"},{"first_name":"Franz","last_name":"Kratochvill","full_name":"Kratochvill, Franz"},{"last_name":"Gratz","first_name":"Nina","full_name":"Gratz, Nina"},{"full_name":"Kenner, Lukas","first_name":"Lukas","last_name":"Kenner"},{"full_name":"Villunger, Andreas","first_name":"Andreas","last_name":"Villunger"},{"full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"},{"full_name":"Kovarik, Pavel","first_name":"Pavel","last_name":"Kovarik"}],"related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"12401"}]},"month":"06","publication_identifier":{"issn":["00219738"]},"quality_controlled":"1","project":[{"name":"The biochemical basis of PAR polarization","call_identifier":"FWF","grant_number":"T00817-B21","_id":"25985A36-B435-11E9-9278-68D0E5697425"},{"grant_number":"P27201-B22","_id":"25E9AF9E-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Revealing the mechanisms underlying drug interactions"}],"oa":1,"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5451238/"}],"external_id":{"pmid":["28504646"]},"language":[{"iso":"eng"}],"doi":"10.1172/JCI80631"},{"day":"01","article_processing_charge":"No","scopus_import":1,"date_published":"2016-12-01T00:00:00Z","publication":"Nature Immunology","citation":{"short":"E. Salzer, D. Çaǧdaş, M. Hons, E. Mace, W. Garncarz, O. Petronczki, R. Platzer, L. Pfajfer, I. Bilic, S. Ban, K. Willmann, M. Mukherjee, V. Supper, H. Hsu, P. Banerjee, P. Sinha, F. Mcclanahan, G. Zlabinger, W. Pickl, J. Gribben, H. Stockinger, K. Bennett, J. Huppa, L. Dupré, Ö. Sanal, U. Jäger, M.K. Sixt, I. Tezcan, J. Orange, K. Boztug, Nature Immunology 17 (2016) 1352–1360.","mla":"Salzer, Elisabeth, et al. “RASGRP1 Deficiency Causes Immunodeficiency with Impaired Cytoskeletal Dynamics.” Nature Immunology, vol. 17, no. 12, Nature Publishing Group, 2016, pp. 1352–60, doi:10.1038/ni.3575.","chicago":"Salzer, Elisabeth, Deniz Çaǧdaş, Miroslav Hons, Emily Mace, Wojciech Garncarz, Oezlem Petronczki, René Platzer, et al. “RASGRP1 Deficiency Causes Immunodeficiency with Impaired Cytoskeletal Dynamics.” Nature Immunology. Nature Publishing Group, 2016. https://doi.org/10.1038/ni.3575.","ama":"Salzer E, Çaǧdaş D, Hons M, et al. RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics. Nature Immunology. 2016;17(12):1352-1360. doi:10.1038/ni.3575","apa":"Salzer, E., Çaǧdaş, D., Hons, M., Mace, E., Garncarz, W., Petronczki, O., … Boztug, K. (2016). RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3575","ieee":"E. Salzer et al., “RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics,” Nature Immunology, vol. 17, no. 12. Nature Publishing Group, pp. 1352–1360, 2016.","ista":"Salzer E, Çaǧdaş D, Hons M, Mace E, Garncarz W, Petronczki O, Platzer R, Pfajfer L, Bilic I, Ban S, Willmann K, Mukherjee M, Supper V, Hsu H, Banerjee P, Sinha P, Mcclanahan F, Zlabinger G, Pickl W, Gribben J, Stockinger H, Bennett K, Huppa J, Dupré L, Sanal Ö, Jäger U, Sixt MK, Tezcan I, Orange J, Boztug K. 2016. RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics. Nature Immunology. 17(12), 1352–1360."},"article_type":"original","page":"1352 - 1360","abstract":[{"text":"RASGRP1 is an important guanine nucleotide exchange factor and activator of the RAS-MAPK pathway following T cell antigen receptor (TCR) signaling. The consequences of RASGRP1 mutations in humans are unknown. In a patient with recurrent bacterial and viral infections, born to healthy consanguineous parents, we used homozygosity mapping and exome sequencing to identify a biallelic stop-gain variant in RASGRP1. This variant segregated perfectly with the disease and has not been reported in genetic databases. RASGRP1 deficiency was associated in T cells and B cells with decreased phosphorylation of the extracellular-signal-regulated serine kinase ERK, which was restored following expression of wild-type RASGRP1. RASGRP1 deficiency also resulted in defective proliferation, activation and motility of T cells and B cells. RASGRP1-deficient natural killer (NK) cells exhibited impaired cytotoxicity with defective granule convergence and actin accumulation. Interaction proteomics identified the dynein light chain DYNLL1 as interacting with RASGRP1, which links RASGRP1 to cytoskeletal dynamics. RASGRP1-deficient cells showed decreased activation of the GTPase RhoA. Treatment with lenalidomide increased RhoA activity and reversed the migration and activation defects of RASGRP1-deficient lymphocytes.","lang":"eng"}],"issue":"12","type":"journal_article","oa_version":"Submitted Version","_id":"1137","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","title":"RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics","intvolume":" 17","month":"12","doi":"10.1038/ni.3575","language":[{"iso":"eng"}],"oa":1,"external_id":{"pmid":["27776107"]},"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6400263","open_access":"1"}],"quality_controlled":"1","publist_id":"6221","author":[{"last_name":"Salzer","first_name":"Elisabeth","full_name":"Salzer, Elisabeth"},{"full_name":"Çaǧdaş, Deniz","first_name":"Deniz","last_name":"Çaǧdaş"},{"full_name":"Hons, Miroslav","orcid":"0000-0002-6625-3348","id":"4167FE56-F248-11E8-B48F-1D18A9856A87","last_name":"Hons","first_name":"Miroslav"},{"first_name":"Emily","last_name":"Mace","full_name":"Mace, Emily"},{"full_name":"Garncarz, Wojciech","first_name":"Wojciech","last_name":"Garncarz"},{"full_name":"Petronczki, Oezlem","last_name":"Petronczki","first_name":"Oezlem"},{"full_name":"Platzer, René","last_name":"Platzer","first_name":"René"},{"full_name":"Pfajfer, Laurène","last_name":"Pfajfer","first_name":"Laurène"},{"full_name":"Bilic, Ivan","last_name":"Bilic","first_name":"Ivan"},{"full_name":"Ban, Sol","last_name":"Ban","first_name":"Sol"},{"last_name":"Willmann","first_name":"Katharina","full_name":"Willmann, Katharina"},{"full_name":"Mukherjee, Malini","first_name":"Malini","last_name":"Mukherjee"},{"last_name":"Supper","first_name":"Verena","full_name":"Supper, Verena"},{"first_name":"Hsiangting","last_name":"Hsu","full_name":"Hsu, Hsiangting"},{"full_name":"Banerjee, Pinaki","first_name":"Pinaki","last_name":"Banerjee"},{"full_name":"Sinha, Papiya","last_name":"Sinha","first_name":"Papiya"},{"full_name":"Mcclanahan, Fabienne","last_name":"Mcclanahan","first_name":"Fabienne"},{"first_name":"Gerhard","last_name":"Zlabinger","full_name":"Zlabinger, Gerhard"},{"first_name":"Winfried","last_name":"Pickl","full_name":"Pickl, Winfried"},{"full_name":"Gribben, John","last_name":"Gribben","first_name":"John"},{"last_name":"Stockinger","first_name":"Hannes","full_name":"Stockinger, Hannes"},{"last_name":"Bennett","first_name":"Keiryn","full_name":"Bennett, Keiryn"},{"full_name":"Huppa, Johannes","first_name":"Johannes","last_name":"Huppa"},{"full_name":"Dupré, Loï̈C","first_name":"Loï̈C","last_name":"Dupré"},{"full_name":"Sanal, Özden","first_name":"Özden","last_name":"Sanal"},{"full_name":"Jäger, Ulrich","first_name":"Ulrich","last_name":"Jäger"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","first_name":"Michael K","last_name":"Sixt","full_name":"Sixt, Michael K"},{"full_name":"Tezcan, Ilhan","last_name":"Tezcan","first_name":"Ilhan"},{"first_name":"Jordan","last_name":"Orange","full_name":"Orange, Jordan"},{"last_name":"Boztug","first_name":"Kaan","full_name":"Boztug, Kaan"}],"date_updated":"2021-01-12T06:48:33Z","date_created":"2018-12-11T11:50:21Z","volume":17,"year":"2016","pmid":1,"publication_status":"published","department":[{"_id":"MiSi"}],"publisher":"Nature Publishing Group"}]