[{"date_published":"2021-04-05T00:00:00Z","doi":"10.1083/jcb.202006081","date_created":"2021-02-05T10:08:04Z","day":"05","publication":"Journal of Cell Biology","has_accepted_license":"1","isi":1,"year":"2021","quality_controlled":"1","publisher":"Rockefeller University Press","oa":1,"title":"Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse","author":[{"first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","last_name":"Leithner","orcid":"0000-0002-1073-744X","full_name":"Leithner, Alexander F"},{"first_name":"LM","full_name":"Altenburger, LM","last_name":"Altenburger"},{"first_name":"R","last_name":"Hauschild","full_name":"Hauschild, R"},{"orcid":"0000-0003-3470-6119","full_name":"Assen, Frank P","last_name":"Assen","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","first_name":"Frank P"},{"first_name":"K","last_name":"Rottner","full_name":"Rottner, K"},{"full_name":"TEB, Stradal","last_name":"TEB","first_name":"Stradal"},{"first_name":"A","full_name":"Diz-Muñoz, A","last_name":"Diz-Muñoz"},{"last_name":"Stein","full_name":"Stein, JV","first_name":"JV"},{"last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"external_id":{"isi":["000626365700001"],"pmid":["33533935"]},"article_processing_charge":"No","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"chicago":"Leithner, Alexander F, LM Altenburger, R Hauschild, Frank P Assen, K Rottner, Stradal TEB, A Diz-Muñoz, JV Stein, and Michael K Sixt. “Dendritic Cell Actin Dynamics Control Contact Duration and Priming Efficiency at the Immunological Synapse.” Journal of Cell Biology. Rockefeller University Press, 2021. https://doi.org/10.1083/jcb.202006081.","ista":"Leithner AF, Altenburger L, Hauschild R, Assen FP, Rottner K, TEB S, Diz-Muñoz A, Stein J, Sixt MK. 2021. Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse. Journal of Cell Biology. 220(4), e202006081.","mla":"Leithner, Alexander F., et al. “Dendritic Cell Actin Dynamics Control Contact Duration and Priming Efficiency at the Immunological Synapse.” Journal of Cell Biology, vol. 220, no. 4, e202006081, Rockefeller University Press, 2021, doi:10.1083/jcb.202006081.","short":"A.F. Leithner, L. Altenburger, R. Hauschild, F.P. Assen, K. Rottner, S. TEB, A. Diz-Muñoz, J. Stein, M.K. Sixt, Journal of Cell Biology 220 (2021).","ieee":"A. F. Leithner et al., “Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse,” Journal of Cell Biology, vol. 220, no. 4. Rockefeller University Press, 2021.","ama":"Leithner AF, Altenburger L, Hauschild R, et al. Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse. Journal of Cell Biology. 2021;220(4). doi:10.1083/jcb.202006081","apa":"Leithner, A. F., Altenburger, L., Hauschild, R., Assen, F. P., Rottner, K., TEB, S., … Sixt, M. K. (2021). Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.202006081"},"article_number":"e202006081","volume":220,"issue":"4","file":[{"file_name":"2021_JournCellBiology_Leithner.pdf","date_created":"2022-05-12T14:16:21Z","creator":"dernst","file_size":5102328,"date_updated":"2022-05-12T14:16:21Z","success":1,"checksum":"843ebc153847c8626e13c9c5ce71d533","file_id":"11367","relation":"main_file","access_level":"open_access","content_type":"application/pdf"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["0021-9525"],"eissn":["1540-8140"]},"publication_status":"published","month":"04","intvolume":" 220","scopus_import":"1","pmid":1,"oa_version":"Published Version","abstract":[{"lang":"eng","text":"Dendritic cells (DCs) are crucial for the priming of naive T cells and the initiation of adaptive immunity. Priming is initiated at a heterologous cell–cell contact, the immunological synapse (IS). While it is established that F-actin dynamics regulates signaling at the T cell side of the contact, little is known about the cytoskeletal contribution on the DC side. Here, we show that the DC actin cytoskeleton is decisive for the formation of a multifocal synaptic structure, which correlates with T cell priming efficiency. DC actin at the IS appears in transient foci that are dynamized by the WAVE regulatory complex (WRC). The absence of the WRC in DCs leads to stabilized contacts with T cells, caused by an increase in ICAM1-integrin–mediated cell–cell adhesion. This results in lower numbers of activated and proliferating T cells, demonstrating an important role for DC actin in the regulation of immune synapse functionality."}],"file_date_updated":"2022-05-12T14:16:21Z","department":[{"_id":"MiSi"}],"ddc":["570"],"date_updated":"2023-09-05T13:57:53Z","status":"public","type":"journal_article","article_type":"original","tmp":{"name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","image":"/images/cc_by_nc_sa.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","short":"CC BY-NC-SA (4.0)"},"_id":"9094"},{"language":[{"iso":"eng"}],"file":[{"success":1,"file_id":"9430","checksum":"337e0f7959c35ec959984cacdcb472ba","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_name":"2021_NatureCommunications_Morandell.pdf","date_created":"2021-05-28T12:39:43Z","file_size":9358599,"date_updated":"2021-05-28T12:39:43Z","creator":"kschuh"}],"publication_status":"published","publication_identifier":{"eissn":["2041-1723"]},"ec_funded":1,"volume":12,"related_material":{"link":[{"url":"https://ist.ac.at/en/news/defective-gene-slows-down-brain-cells/","relation":"press_release"}],"record":[{"id":"7800","status":"public","relation":"earlier_version"},{"id":"12401","status":"public","relation":"dissertation_contains"}]},"issue":"1","oa_version":"Published Version","acknowledged_ssus":[{"_id":"PreCl"}],"abstract":[{"text":"De novo loss of function mutations in the ubiquitin ligase-encoding gene Cullin3 lead to autism spectrum disorder (ASD). In mouse, constitutive haploinsufficiency leads to motor coordination deficits as well as ASD-relevant social and cognitive impairments. However, induction of Cul3 haploinsufficiency later in life does not lead to ASD-relevant behaviors, pointing to an important role of Cul3 during a critical developmental window. Here we show that Cul3 is essential to regulate neuronal migration and, therefore, constitutive Cul3 heterozygous mutant mice display cortical lamination abnormalities. At the molecular level, we found that Cul3 controls neuronal migration by tightly regulating the amount of Plastin3 (Pls3), a previously unrecognized player of neural migration. Furthermore, we found that Pls3 cell-autonomously regulates cell migration by regulating actin cytoskeleton organization, and its levels are inversely proportional to neural migration speed. Finally, we provide evidence that cellular phenotypes associated with autism-linked gene haploinsufficiency can be rescued by transcriptional activation of the intact allele in vitro, offering a proof of concept for a potential therapeutic approach for ASDs.","lang":"eng"}],"intvolume":" 12","month":"05","ddc":["572"],"date_updated":"2024-03-27T23:30:23Z","file_date_updated":"2021-05-28T12:39:43Z","department":[{"_id":"GaNo"},{"_id":"JoDa"},{"_id":"FlSc"},{"_id":"MiSi"},{"_id":"LifeSc"},{"_id":"Bio"}],"_id":"9429","keyword":["General Biochemistry","Genetics and Molecular Biology"],"status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"original","publication":"Nature Communications","day":"24","year":"2021","has_accepted_license":"1","isi":1,"date_created":"2021-05-28T11:49:46Z","doi":"10.1038/s41467-021-23123-x","date_published":"2021-05-24T00:00:00Z","acknowledgement":"We thank A. Coll Manzano, F. Freeman, M. Ladron de Guevara, and A. Ç. Yahya for technical assistance, S. Deixler, A. Lepold, and A. Schlerka for the management of our animal colony, as well as M. Schunn and the Preclinical Facility team for technical assistance. We thank K. Heesom and her team at the University of Bristol Proteomics Facility for the proteomics sample preparation, data generation, and analysis support. We thank Y. B. Simon for kindly providing the plasmid for lentiviral labeling. Further, we thank M. Sixt for his advice regarding cell migration and the fruitful discussions. This work was supported by the ISTPlus postdoctoral fellowship (Grant Agreement No. 754411) to B.B., by the European Union’s Horizon 2020 research and innovation program (ERC) grant 715508 (REVERSEAUTISM), and by the Austrian Science Fund (FWF) to G.N. (DK W1232-B24 and SFB F7807-B) and to J.G.D (I3600-B27).","oa":1,"publisher":"Springer Nature","quality_controlled":"1","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ista":"Morandell J, Schwarz LA, Basilico B, Tasciyan S, Dimchev GA, Nicolas A, Sommer CM, Kreuzinger C, Dotter C, Knaus L, Dobler Z, Cacci E, Schur FK, Danzl JG, Novarino G. 2021. Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development. Nature Communications. 12(1), 3058.","chicago":"Morandell, Jasmin, Lena A Schwarz, Bernadette Basilico, Saren Tasciyan, Georgi A Dimchev, Armel Nicolas, Christoph M Sommer, et al. “Cul3 Regulates Cytoskeleton Protein Homeostasis and Cell Migration during a Critical Window of Brain Development.” Nature Communications. Springer Nature, 2021. https://doi.org/10.1038/s41467-021-23123-x.","ama":"Morandell J, Schwarz LA, Basilico B, et al. Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development. Nature Communications. 2021;12(1). doi:10.1038/s41467-021-23123-x","apa":"Morandell, J., Schwarz, L. A., Basilico, B., Tasciyan, S., Dimchev, G. A., Nicolas, A., … Novarino, G. (2021). Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-021-23123-x","short":"J. Morandell, L.A. Schwarz, B. Basilico, S. Tasciyan, G.A. Dimchev, A. Nicolas, C.M. Sommer, C. Kreuzinger, C. Dotter, L. Knaus, Z. Dobler, E. Cacci, F.K. Schur, J.G. Danzl, G. Novarino, Nature Communications 12 (2021).","ieee":"J. Morandell et al., “Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development,” Nature Communications, vol. 12, no. 1. Springer Nature, 2021.","mla":"Morandell, Jasmin, et al. “Cul3 Regulates Cytoskeleton Protein Homeostasis and Cell Migration during a Critical Window of Brain Development.” Nature Communications, vol. 12, no. 1, 3058, Springer Nature, 2021, doi:10.1038/s41467-021-23123-x."},"title":"Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development","article_processing_charge":"No","external_id":{"isi":["000658769900010"]},"author":[{"first_name":"Jasmin","id":"4739D480-F248-11E8-B48F-1D18A9856A87","last_name":"Morandell","full_name":"Morandell, Jasmin"},{"id":"29A8453C-F248-11E8-B48F-1D18A9856A87","first_name":"Lena A","full_name":"Schwarz, Lena A","last_name":"Schwarz"},{"first_name":"Bernadette","id":"36035796-5ACA-11E9-A75E-7AF2E5697425","last_name":"Basilico","full_name":"Basilico, Bernadette","orcid":"0000-0003-1843-3173"},{"id":"4323B49C-F248-11E8-B48F-1D18A9856A87","first_name":"Saren","last_name":"Tasciyan","orcid":"0000-0003-1671-393X","full_name":"Tasciyan, Saren"},{"first_name":"Georgi A","id":"38C393BE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8370-6161","full_name":"Dimchev, Georgi A","last_name":"Dimchev"},{"id":"2A103192-F248-11E8-B48F-1D18A9856A87","first_name":"Armel","full_name":"Nicolas, Armel","last_name":"Nicolas"},{"first_name":"Christoph M","id":"4DF26D8C-F248-11E8-B48F-1D18A9856A87","last_name":"Sommer","orcid":"0000-0003-1216-9105","full_name":"Sommer, Christoph M"},{"id":"382077BA-F248-11E8-B48F-1D18A9856A87","first_name":"Caroline","full_name":"Kreuzinger, Caroline","last_name":"Kreuzinger"},{"first_name":"Christoph","id":"4C66542E-F248-11E8-B48F-1D18A9856A87","last_name":"Dotter","orcid":"0000-0002-9033-9096","full_name":"Dotter, Christoph"},{"id":"3B2ABCF4-F248-11E8-B48F-1D18A9856A87","first_name":"Lisa","full_name":"Knaus, Lisa","last_name":"Knaus"},{"last_name":"Dobler","full_name":"Dobler, Zoe","id":"D23090A2-9057-11EA-883A-A8396FC7A38F","first_name":"Zoe"},{"last_name":"Cacci","full_name":"Cacci, Emanuele","first_name":"Emanuele"},{"first_name":"Florian KM","id":"48AD8942-F248-11E8-B48F-1D18A9856A87","last_name":"Schur","orcid":"0000-0003-4790-8078","full_name":"Schur, Florian KM"},{"last_name":"Danzl","full_name":"Danzl, Johann G","orcid":"0000-0001-8559-3973","id":"42EFD3B6-F248-11E8-B48F-1D18A9856A87","first_name":"Johann G"},{"full_name":"Novarino, Gaia","orcid":"0000-0002-7673-7178","last_name":"Novarino","first_name":"Gaia","id":"3E57A680-F248-11E8-B48F-1D18A9856A87"}],"article_number":"3058","project":[{"_id":"260C2330-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","name":"ISTplus - Postdoctoral Fellowships","grant_number":"754411"},{"call_identifier":"H2020","_id":"25444568-B435-11E9-9278-68D0E5697425","name":"Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo and in vitro Models","grant_number":"715508"},{"_id":"2548AE96-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"W1232-B24","name":"Molecular Drug Targets"},{"_id":"05A0D778-7A3F-11EA-A408-12923DDC885E","name":"Neural stem cells in autism and epilepsy","grant_number":"F07807"},{"call_identifier":"FWF","_id":"265CB4D0-B435-11E9-9278-68D0E5697425","grant_number":"I03600","name":"Optical control of synaptic function via adhesion molecules"}]},{"acknowledged_ssus":[{"_id":"LifeSc"},{"_id":"Bio"},{"_id":"PreCl"},{"_id":"EM-Fac"}],"abstract":[{"lang":"eng","text":"Bacteria-host interactions represent a continuous trade-off between benefit and risk. Thus, the host immune response is faced with a non-trivial problem – accommodate beneficial commensals and remove harmful pathogens. This is especially difficult as molecular patterns, such as lipopolysaccharide or specific surface organelles such as pili, are conserved in both, commensal and pathogenic bacteria. Type 1 pili, tightly regulated by phase variation, are considered an important virulence factor of pathogenic bacteria as they facilitate invasion into host cells. While invasion represents a de facto passive mechanism for pathogens to escape the host immune response, we demonstrate a fundamental role of type 1 pili as active modulators of the innate and adaptive immune response."}],"oa_version":"Published Version","alternative_title":["ISTA Thesis"],"month":"11","degree_awarded":"PhD","publication_status":"published","publication_identifier":{"issn":["2663-337X"]},"language":[{"iso":"eng"}],"file":[{"content_type":"application/pdf","access_level":"open_access","relation":"main_file","checksum":"b39c9e0ef18d0484d537a67551effd02","file_id":"10308","embargo":"2022-11-18","date_updated":"2022-12-20T23:30:05Z","file_size":13266088,"creator":"ktomasek","date_created":"2021-11-18T15:07:31Z","file_name":"ThesisTomasekKathrin.pdf"},{"creator":"ktomasek","date_updated":"2022-12-20T23:30:05Z","file_size":7539509,"date_created":"2021-11-18T15:07:46Z","file_name":"ThesisTomasekKathrin.docx","access_level":"closed","relation":"source_file","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","embargo_to":"open_access","file_id":"10309","checksum":"c0c440ee9e5ef1102a518a4f9f023e7c"}],"related_material":{"record":[{"relation":"part_of_dissertation","status":"public","id":"10316"}]},"_id":"10307","type":"dissertation","status":"public","date_updated":"2023-09-07T13:34:38Z","supervisor":[{"orcid":"0000-0002-4561-241X","full_name":"Sixt, Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"},{"last_name":"Guet","full_name":"Guet, Calin C","orcid":"0000-0001-6220-2052","first_name":"Calin C","id":"47F8433E-F248-11E8-B48F-1D18A9856A87"}],"ddc":["570"],"file_date_updated":"2022-12-20T23:30:05Z","department":[{"_id":"MiSi"},{"_id":"CaGu"},{"_id":"GradSch"}],"oa":1,"publisher":"Institute of Science and Technology Austria","year":"2021","has_accepted_license":"1","day":"18","page":"73","date_created":"2021-11-18T15:05:06Z","doi":"10.15479/at:ista:10307","date_published":"2021-11-18T00:00:00Z","citation":{"ieee":"K. Tomasek, “Pathogenic Escherichia coli hijack the host immune response,” Institute of Science and Technology Austria, 2021.","short":"K. Tomasek, Pathogenic Escherichia Coli Hijack the Host Immune Response, Institute of Science and Technology Austria, 2021.","apa":"Tomasek, K. (2021). Pathogenic Escherichia coli hijack the host immune response. Institute of Science and Technology Austria. https://doi.org/10.15479/at:ista:10307","ama":"Tomasek K. Pathogenic Escherichia coli hijack the host immune response. 2021. doi:10.15479/at:ista:10307","mla":"Tomasek, Kathrin. Pathogenic Escherichia Coli Hijack the Host Immune Response. Institute of Science and Technology Austria, 2021, doi:10.15479/at:ista:10307.","ista":"Tomasek K. 2021. Pathogenic Escherichia coli hijack the host immune response. Institute of Science and Technology Austria.","chicago":"Tomasek, Kathrin. “Pathogenic Escherichia Coli Hijack the Host Immune Response.” Institute of Science and Technology Austria, 2021. https://doi.org/10.15479/at:ista:10307."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","article_processing_charge":"No","author":[{"first_name":"Kathrin","id":"3AEC8556-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-3768-877X","full_name":"Tomasek, Kathrin","last_name":"Tomasek"}],"title":"Pathogenic Escherichia coli hijack the host immune response"},{"acknowledgement":"We thank Ulrich Dobrindt for providing UPEC strain CFT073, Vlad Gavra and Maximilian Götz, Bor Kavčič, Jonna Alanko and Eva Kiermaier for help with experiments and Robert Hauschild, Julian Stopp and Saren Tasciyan for help with data analysis. We thank the IST Austria Scientific Service Units, especially the Bioimaging facility, the Preclinical facility and the Electron microscopy facility for technical support, Jakob Wallner and all members of the Guet and Sixt lab for fruitful discussions and Daria Siekhaus for critically reading the manuscript. This work was supported by grants from the Austrian Research Promotion Agency (FEMtech 868984) to I.G., the European Research Council (CoG 724373) and the Austrian Science Fund (FWF P29911) to M.S.","oa_version":"Preprint","abstract":[{"lang":"eng","text":"A key attribute of persistent or recurring bacterial infections is the ability of the pathogen to evade the host’s immune response. Many Enterobacteriaceae express type 1 pili, a pre-adapted virulence trait, to invade host epithelial cells and establish persistent infections. However, the molecular mechanisms and strategies by which bacteria actively circumvent the immune response of the host remain poorly understood. Here, we identified CD14, the major co-receptor for lipopolysaccharide detection, on dendritic cells as a previously undescribed binding partner of FimH, the protein located at the tip of the type 1 pilus of Escherichia coli. The FimH amino acids involved in CD14 binding are highly conserved across pathogenic and non-pathogenic strains. Binding of pathogenic bacteria to CD14 lead to reduced dendritic cell migration and blunted expression of co-stimulatory molecules, both rate-limiting factors of T cell activation. While defining an active molecular mechanism of immune evasion by pathogens, the interaction between FimH and CD14 represents a potential target to interfere with persistent and recurrent infections, such as urinary tract infections or Crohn’s disease."}],"acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"},{"_id":"EM-Fac"}],"month":"10","main_file_link":[{"open_access":"1","url":"https://www.biorxiv.org/content/10.1101/2021.10.18.464770v1"}],"oa":1,"publisher":"Cold Spring Harbor Laboratory","publication":"bioRxiv","language":[{"iso":"eng"}],"day":"18","year":"2021","publication_status":"submitted","ec_funded":1,"date_created":"2021-11-19T12:24:16Z","related_material":{"record":[{"relation":"later_version","id":"11843","status":"public"},{"id":"10307","status":"public","relation":"dissertation_contains"}]},"doi":"10.1101/2021.10.18.464770","date_published":"2021-10-18T00:00:00Z","_id":"10316","project":[{"grant_number":"724373","name":"Cellular navigation along spatial gradients","call_identifier":"H2020","_id":"25FE9508-B435-11E9-9278-68D0E5697425"},{"name":"Mechanical adaptation of lamellipodial actin","grant_number":"P29911","_id":"26018E70-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"status":"public","type":"preprint","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","citation":{"mla":"Tomasek, Kathrin, et al. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack the Host Immune Response by Binding to CD14.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2021.10.18.464770.","short":"K. Tomasek, A.F. Leithner, I. Glatzová, M.S. Lukesch, C.C. Guet, M.K. Sixt, BioRxiv (n.d.).","ieee":"K. Tomasek, A. F. Leithner, I. Glatzová, M. S. Lukesch, C. C. Guet, and M. K. Sixt, “Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14,” bioRxiv. Cold Spring Harbor Laboratory.","ama":"Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. bioRxiv. doi:10.1101/2021.10.18.464770","apa":"Tomasek, K., Leithner, A. F., Glatzová, I., Lukesch, M. S., Guet, C. C., & Sixt, M. K. (n.d.). Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. bioRxiv. Cold Spring Harbor Laboratory. https://doi.org/10.1101/2021.10.18.464770","chicago":"Tomasek, Kathrin, Alexander F Leithner, Ivana Glatzová, Michael S. Lukesch, Calin C Guet, and Michael K Sixt. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack the Host Immune Response by Binding to CD14.” BioRxiv. Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2021.10.18.464770.","ista":"Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. bioRxiv, 10.1101/2021.10.18.464770."},"date_updated":"2024-03-27T23:30:35Z","title":"Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14","department":[{"_id":"CaGu"},{"_id":"MiSi"}],"article_processing_charge":"No","author":[{"last_name":"Tomasek","orcid":"0000-0003-3768-877X","full_name":"Tomasek, Kathrin","id":"3AEC8556-F248-11E8-B48F-1D18A9856A87","first_name":"Kathrin"},{"id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander F","full_name":"Leithner, Alexander F","orcid":"0000-0002-1073-744X","last_name":"Leithner"},{"first_name":"Ivana","id":"727b3c7d-4939-11ec-89b3-b9b0750ab74d","full_name":"Glatzová, Ivana","last_name":"Glatzová"},{"first_name":"Michael S.","last_name":"Lukesch","full_name":"Lukesch, Michael S."},{"id":"47F8433E-F248-11E8-B48F-1D18A9856A87","first_name":"Calin C","orcid":"0000-0001-6220-2052","full_name":"Guet, Calin C","last_name":"Guet"},{"full_name":"Sixt, Michael K","orcid":"0000-0002-4561-241X","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}]},{"isi":1,"has_accepted_license":"1","year":"2020","day":"01","publication":"Immunology and Cell Biology","page":"93-113","date_published":"2020-02-01T00:00:00Z","doi":"10.1111/imcb.12304","date_created":"2020-01-05T23:00:48Z","publisher":"Wiley","quality_controlled":"1","oa":1,"citation":{"ista":"Obeidy P, Ju LA, Oehlers SH, Zulkhernain NS, Lee Q, Galeano Niño JL, Kwan RYQ, Tikoo S, Cavanagh LL, Mrass P, Cook AJL, Jackson SP, Biro M, Roediger B, Sixt MK, Weninger W. 2020. Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes. Immunology and Cell Biology. 98(2), 93–113.","chicago":"Obeidy, Peyman, Lining A. Ju, Stefan H. Oehlers, Nursafwana S. Zulkhernain, Quintin Lee, Jorge L. Galeano Niño, Rain Y.Q. Kwan, et al. “Partial Loss of Actin Nucleator Actin-Related Protein 2/3 Activity Triggers Blebbing in Primary T Lymphocytes.” Immunology and Cell Biology. Wiley, 2020. https://doi.org/10.1111/imcb.12304.","ieee":"P. Obeidy et al., “Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes,” Immunology and Cell Biology, vol. 98, no. 2. Wiley, pp. 93–113, 2020.","short":"P. Obeidy, L.A. Ju, S.H. Oehlers, N.S. Zulkhernain, Q. Lee, J.L. Galeano Niño, R.Y.Q. Kwan, S. Tikoo, L.L. Cavanagh, P. Mrass, A.J.L. Cook, S.P. Jackson, M. Biro, B. Roediger, M.K. Sixt, W. Weninger, Immunology and Cell Biology 98 (2020) 93–113.","apa":"Obeidy, P., Ju, L. A., Oehlers, S. H., Zulkhernain, N. S., Lee, Q., Galeano Niño, J. L., … Weninger, W. (2020). Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes. Immunology and Cell Biology. Wiley. https://doi.org/10.1111/imcb.12304","ama":"Obeidy P, Ju LA, Oehlers SH, et al. Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes. Immunology and Cell Biology. 2020;98(2):93-113. doi:10.1111/imcb.12304","mla":"Obeidy, Peyman, et al. “Partial Loss of Actin Nucleator Actin-Related Protein 2/3 Activity Triggers Blebbing in Primary T Lymphocytes.” Immunology and Cell Biology, vol. 98, no. 2, Wiley, 2020, pp. 93–113, doi:10.1111/imcb.12304."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","author":[{"first_name":"Peyman","last_name":"Obeidy","full_name":"Obeidy, Peyman"},{"full_name":"Ju, Lining A.","last_name":"Ju","first_name":"Lining A."},{"first_name":"Stefan H.","last_name":"Oehlers","full_name":"Oehlers, Stefan H."},{"last_name":"Zulkhernain","full_name":"Zulkhernain, Nursafwana S.","first_name":"Nursafwana S."},{"full_name":"Lee, Quintin","last_name":"Lee","first_name":"Quintin"},{"last_name":"Galeano Niño","full_name":"Galeano Niño, Jorge L.","first_name":"Jorge L."},{"first_name":"Rain Y.Q.","last_name":"Kwan","full_name":"Kwan, Rain Y.Q."},{"last_name":"Tikoo","full_name":"Tikoo, Shweta","first_name":"Shweta"},{"first_name":"Lois L.","full_name":"Cavanagh, Lois L.","last_name":"Cavanagh"},{"full_name":"Mrass, Paulus","last_name":"Mrass","first_name":"Paulus"},{"last_name":"Cook","full_name":"Cook, Adam J.L.","first_name":"Adam J.L."},{"first_name":"Shaun P.","full_name":"Jackson, Shaun P.","last_name":"Jackson"},{"full_name":"Biro, Maté","last_name":"Biro","first_name":"Maté"},{"first_name":"Ben","last_name":"Roediger","full_name":"Roediger, Ben"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt"},{"first_name":"Wolfgang","full_name":"Weninger, Wolfgang","last_name":"Weninger"}],"article_processing_charge":"No","external_id":{"pmid":["31698518"],"isi":["000503885600001"]},"title":"Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes","publication_identifier":{"eissn":["14401711"],"issn":["08189641"]},"publication_status":"published","file":[{"access_level":"open_access","relation":"main_file","content_type":"application/pdf","file_id":"8775","checksum":"c389477b4b52172ef76afff8a06c6775","success":1,"creator":"dernst","date_updated":"2020-11-19T11:22:33Z","file_size":8569945,"date_created":"2020-11-19T11:22:33Z","file_name":"2020_ImmunologyCellBio_Obeidy.pdf"}],"language":[{"iso":"eng"}],"volume":98,"issue":"2","abstract":[{"lang":"eng","text":"T lymphocytes utilize amoeboid migration to navigate effectively within complex microenvironments. The precise rearrangement of the actin cytoskeleton required for cellular forward propulsion is mediated by actin regulators, including the actin‐related protein 2/3 (Arp2/3) complex, a macromolecular machine that nucleates branched actin filaments at the leading edge. The consequences of modulating Arp2/3 activity on the biophysical properties of the actomyosin cortex and downstream T cell function are incompletely understood. We report that even a moderate decrease of Arp3 levels in T cells profoundly affects actin cortex integrity. Reduction in total F‐actin content leads to reduced cortical tension and disrupted lamellipodia formation. Instead, in Arp3‐knockdown cells, the motility mode is dominated by blebbing migration characterized by transient, balloon‐like protrusions at the leading edge. Although this migration mode seems to be compatible with interstitial migration in three‐dimensional environments, diminished locomotion kinetics and impaired cytotoxicity interfere with optimal T cell function. These findings define the importance of finely tuned, Arp2/3‐dependent mechanophysical membrane integrity in cytotoxic effector T lymphocyte activities."}],"oa_version":"Published Version","pmid":1,"scopus_import":"1","month":"02","intvolume":" 98","date_updated":"2023-08-17T14:21:12Z","ddc":["570"],"department":[{"_id":"MiSi"}],"file_date_updated":"2020-11-19T11:22:33Z","_id":"7234","article_type":"original","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public"},{"page":"513-537","date_published":"2020-03-18T00:00:00Z","doi":"10.1142/S021820252050013X","date_created":"2020-03-31T11:25:05Z","isi":1,"year":"2020","day":"18","publication":"Mathematical Models and Methods in Applied Sciences","quality_controlled":"1","publisher":"World Scientific","oa":1,"acknowledgement":"This work has been supported by the Vienna Science and Technology Fund, Grant no. LS13-029. G.J. and C.S. also acknowledge support by the Austrian Science Fund, Grants no. W1245, F 65, and W1261, as well as by the Fondation Sciences Mathématiques de Paris, and by Paris-Sciences-et-Lettres.","author":[{"last_name":"Jankowiak","full_name":"Jankowiak, Gaspard","first_name":"Gaspard"},{"full_name":"Peurichard, Diane","last_name":"Peurichard","first_name":"Diane"},{"orcid":"0000-0003-0666-8928","full_name":"Reversat, Anne","last_name":"Reversat","first_name":"Anne","id":"35B76592-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Schmeiser, Christian","last_name":"Schmeiser","first_name":"Christian"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"}],"article_processing_charge":"No","external_id":{"isi":["000525349900003"],"arxiv":["1903.09426"]},"title":"Modeling adhesion-independent cell migration","citation":{"ama":"Jankowiak G, Peurichard D, Reversat A, Schmeiser C, Sixt MK. Modeling adhesion-independent cell migration. Mathematical Models and Methods in Applied Sciences. 2020;30(3):513-537. doi:10.1142/S021820252050013X","apa":"Jankowiak, G., Peurichard, D., Reversat, A., Schmeiser, C., & Sixt, M. K. (2020). Modeling adhesion-independent cell migration. Mathematical Models and Methods in Applied Sciences. World Scientific. https://doi.org/10.1142/S021820252050013X","short":"G. Jankowiak, D. Peurichard, A. Reversat, C. Schmeiser, M.K. Sixt, Mathematical Models and Methods in Applied Sciences 30 (2020) 513–537.","ieee":"G. Jankowiak, D. Peurichard, A. Reversat, C. Schmeiser, and M. K. Sixt, “Modeling adhesion-independent cell migration,” Mathematical Models and Methods in Applied Sciences, vol. 30, no. 3. World Scientific, pp. 513–537, 2020.","mla":"Jankowiak, Gaspard, et al. “Modeling Adhesion-Independent Cell Migration.” Mathematical Models and Methods in Applied Sciences, vol. 30, no. 3, World Scientific, 2020, pp. 513–37, doi:10.1142/S021820252050013X.","ista":"Jankowiak G, Peurichard D, Reversat A, Schmeiser C, Sixt MK. 2020. Modeling adhesion-independent cell migration. Mathematical Models and Methods in Applied Sciences. 30(3), 513–537.","chicago":"Jankowiak, Gaspard, Diane Peurichard, Anne Reversat, Christian Schmeiser, and Michael K Sixt. “Modeling Adhesion-Independent Cell Migration.” Mathematical Models and Methods in Applied Sciences. World Scientific, 2020. https://doi.org/10.1142/S021820252050013X."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","project":[{"grant_number":"LS13-029","name":"Modeling of Polarization and Motility of Leukocytes in Three-Dimensional Environments","_id":"25AD6156-B435-11E9-9278-68D0E5697425"}],"issue":"3","volume":30,"publication_identifier":{"issn":["02182025"]},"publication_status":"published","language":[{"iso":"eng"}],"scopus_import":"1","main_file_link":[{"open_access":"1","url":"https://arxiv.org/abs/1903.09426"}],"month":"03","intvolume":" 30","abstract":[{"lang":"eng","text":"A two-dimensional mathematical model for cells migrating without adhesion capabilities is presented and analyzed. Cells are represented by their cortex, which is modeled as an elastic curve, subject to an internal pressure force. Net polymerization or depolymerization in the cortex is modeled via local addition or removal of material, driving a cortical flow. The model takes the form of a fully nonlinear degenerate parabolic system. An existence analysis is carried out by adapting ideas from the theory of gradient flows. Numerical simulations show that these simple rules can account for the behavior observed in experiments, suggesting a possible mechanical mechanism for adhesion-independent motility."}],"oa_version":"Preprint","department":[{"_id":"MiSi"}],"date_updated":"2023-08-18T10:18:56Z","type":"journal_article","article_type":"original","status":"public","_id":"7623"},{"department":[{"_id":"MiSi"},{"_id":"Bio"},{"_id":"NanoFab"}],"file_date_updated":"2020-11-24T13:25:13Z","date_updated":"2023-08-21T06:28:17Z","ddc":["570"],"article_type":"original","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","_id":"7875","volume":219,"issue":"6","ec_funded":1,"publication_identifier":{"eissn":["1540-8140"]},"publication_status":"published","file":[{"checksum":"cb0b9c77842ae1214caade7b77e4d82d","file_id":"8801","success":1,"content_type":"application/pdf","access_level":"open_access","relation":"main_file","date_created":"2020-11-24T13:25:13Z","file_name":"2020_JCellBiol_Kopf.pdf","date_updated":"2020-11-24T13:25:13Z","file_size":7536712,"creator":"dernst"}],"language":[{"iso":"eng"}],"scopus_import":"1","month":"06","intvolume":" 219","abstract":[{"lang":"eng","text":"Cells navigating through complex tissues face a fundamental challenge: while multiple protrusions explore different paths, the cell needs to avoid entanglement. How a cell surveys and then corrects its own shape is poorly understood. Here, we demonstrate that spatially distinct microtubule dynamics regulate amoeboid cell migration by locally promoting the retraction of protrusions. In migrating dendritic cells, local microtubule depolymerization within protrusions remote from the microtubule organizing center triggers actomyosin contractility controlled by RhoA and its exchange factor Lfc. Depletion of Lfc leads to aberrant myosin localization, thereby causing two effects that rate-limit locomotion: (1) impaired cell edge coordination during path finding and (2) defective adhesion resolution. Compromised shape control is particularly hindering in geometrically complex microenvironments, where it leads to entanglement and ultimately fragmentation of the cell body. We thus demonstrate that microtubules can act as a proprioceptive device: they sense cell shape and control actomyosin retraction to sustain cellular coherence."}],"acknowledged_ssus":[{"_id":"LifeSc"},{"_id":"Bio"},{"_id":"PreCl"}],"pmid":1,"oa_version":"Published Version","author":[{"id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87","first_name":"Aglaja","full_name":"Kopf, Aglaja","orcid":"0000-0002-2187-6656","last_name":"Kopf"},{"orcid":"0000-0003-2856-3369","full_name":"Renkawitz, Jörg","last_name":"Renkawitz","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","first_name":"Jörg"},{"orcid":"0000-0001-9843-3522","full_name":"Hauschild, Robert","last_name":"Hauschild","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","first_name":"Robert"},{"last_name":"Girkontaite","full_name":"Girkontaite, Irute","first_name":"Irute"},{"first_name":"Kerry","last_name":"Tedford","full_name":"Tedford, Kerry"},{"id":"4515C308-F248-11E8-B48F-1D18A9856A87","first_name":"Jack","last_name":"Merrin","full_name":"Merrin, Jack","orcid":"0000-0001-5145-4609"},{"full_name":"Thorn-Seshold, Oliver","last_name":"Thorn-Seshold","first_name":"Oliver"},{"last_name":"Trauner","full_name":"Trauner, Dirk","id":"E8F27F48-3EBA-11E9-92A1-B709E6697425","first_name":"Dirk"},{"last_name":"Häcker","full_name":"Häcker, Hans","first_name":"Hans"},{"last_name":"Fischer","full_name":"Fischer, Klaus Dieter","first_name":"Klaus Dieter"},{"last_name":"Kiermaier","full_name":"Kiermaier, Eva","orcid":"0000-0001-6165-5738","first_name":"Eva","id":"3EB04B78-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}],"external_id":{"isi":["000538141100020"],"pmid":["32379884"]},"article_processing_charge":"No","title":"Microtubules control cellular shape and coherence in amoeboid migrating cells","citation":{"short":"A. Kopf, J. Renkawitz, R. Hauschild, I. Girkontaite, K. Tedford, J. Merrin, O. Thorn-Seshold, D. Trauner, H. Häcker, K.D. Fischer, E. Kiermaier, M.K. Sixt, The Journal of Cell Biology 219 (2020).","ieee":"A. Kopf et al., “Microtubules control cellular shape and coherence in amoeboid migrating cells,” The Journal of Cell Biology, vol. 219, no. 6. Rockefeller University Press, 2020.","ama":"Kopf A, Renkawitz J, Hauschild R, et al. Microtubules control cellular shape and coherence in amoeboid migrating cells. The Journal of Cell Biology. 2020;219(6). doi:10.1083/jcb.201907154","apa":"Kopf, A., Renkawitz, J., Hauschild, R., Girkontaite, I., Tedford, K., Merrin, J., … Sixt, M. K. (2020). Microtubules control cellular shape and coherence in amoeboid migrating cells. The Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201907154","mla":"Kopf, Aglaja, et al. “Microtubules Control Cellular Shape and Coherence in Amoeboid Migrating Cells.” The Journal of Cell Biology, vol. 219, no. 6, e201907154, Rockefeller University Press, 2020, doi:10.1083/jcb.201907154.","ista":"Kopf A, Renkawitz J, Hauschild R, Girkontaite I, Tedford K, Merrin J, Thorn-Seshold O, Trauner D, Häcker H, Fischer KD, Kiermaier E, Sixt MK. 2020. Microtubules control cellular shape and coherence in amoeboid migrating cells. The Journal of Cell Biology. 219(6), e201907154.","chicago":"Kopf, Aglaja, Jörg Renkawitz, Robert Hauschild, Irute Girkontaite, Kerry Tedford, Jack Merrin, Oliver Thorn-Seshold, et al. “Microtubules Control Cellular Shape and Coherence in Amoeboid Migrating Cells.” The Journal of Cell Biology. Rockefeller University Press, 2020. https://doi.org/10.1083/jcb.201907154."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","project":[{"_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes","grant_number":"281556"},{"name":"Cellular navigation along spatial gradients","grant_number":"724373","call_identifier":"H2020","_id":"25FE9508-B435-11E9-9278-68D0E5697425"},{"grant_number":"P29911","name":"Mechanical adaptation of lamellipodial actin","call_identifier":"FWF","_id":"26018E70-B435-11E9-9278-68D0E5697425"},{"_id":"252C3B08-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Nano-Analytics of Cellular Systems","grant_number":"W 1250-B20"},{"name":"International IST Postdoc Fellowship Programme","grant_number":"291734","_id":"25681D80-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"grant_number":"ALTF 1396-2014","name":"Molecular and system level view of immune cell migration","_id":"25A48D24-B435-11E9-9278-68D0E5697425"}],"article_number":"e201907154","doi":"10.1083/jcb.201907154","date_published":"2020-06-01T00:00:00Z","date_created":"2020-05-24T22:00:56Z","has_accepted_license":"1","isi":1,"year":"2020","day":"01","publication":"The Journal of Cell Biology","publisher":"Rockefeller University Press","quality_controlled":"1","oa":1,"acknowledgement":"The authors thank the Scientific Service Units (Life Sciences, Bioimaging, Preclinical) of the Institute of Science and Technology Austria for excellent support. This work was funded by the European Research Council (ERC StG 281556 and CoG 724373), two grants from the Austrian\r\nScience Fund (FWF; P29911 and DK Nanocell W1250-B20 to M. Sixt) and by the German Research Foundation (DFG SFB1032 project B09) to O. Thorn-Seshold and D. Trauner. J. Renkawitz was supported by ISTFELLOW funding from the People Program (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) under the Research Executive Agency grant agreement (291734) and a European Molecular Biology Organization long-term fellowship (ALTF 1396-2014) co-funded by the European Commission (LTFCOFUND2013, GA-2013-609409), E. Kiermaier by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany’s Excellence Strategy—EXC 2151—390873048, and H. Hacker by the American Lebanese Syrian Associated ¨Charities. K.-D. Fischer was supported by the Analysis, Imaging and Modelling of Neuronal and Inflammatory Processes graduate school funded by the Ministry of Economics, Science, and Digitisation of the State Saxony-Anhalt and by the European Funds for Social and Regional Development."},{"quality_controlled":"1","publisher":"Elsevier","oa":1,"day":"19","publication":"Immunity","isi":1,"year":"2020","doi":"10.1016/j.immuni.2020.04.020","date_published":"2020-05-19T00:00:00Z","date_created":"2020-05-24T22:00:57Z","page":"721-723","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ista":"Sixt MK, Lämmermann T. 2020. T cells: Bridge-and-channel commute to the white pulp. Immunity. 52(5), 721–723.","chicago":"Sixt, Michael K, and Tim Lämmermann. “T Cells: Bridge-and-Channel Commute to the White Pulp.” Immunity. Elsevier, 2020. https://doi.org/10.1016/j.immuni.2020.04.020.","ieee":"M. K. Sixt and T. Lämmermann, “T cells: Bridge-and-channel commute to the white pulp,” Immunity, vol. 52, no. 5. Elsevier, pp. 721–723, 2020.","short":"M.K. Sixt, T. Lämmermann, Immunity 52 (2020) 721–723.","ama":"Sixt MK, Lämmermann T. T cells: Bridge-and-channel commute to the white pulp. Immunity. 2020;52(5):721-723. doi:10.1016/j.immuni.2020.04.020","apa":"Sixt, M. K., & Lämmermann, T. (2020). T cells: Bridge-and-channel commute to the white pulp. Immunity. Elsevier. https://doi.org/10.1016/j.immuni.2020.04.020","mla":"Sixt, Michael K., and Tim Lämmermann. “T Cells: Bridge-and-Channel Commute to the White Pulp.” Immunity, vol. 52, no. 5, Elsevier, 2020, pp. 721–23, doi:10.1016/j.immuni.2020.04.020."},"title":"T cells: Bridge-and-channel commute to the white pulp","author":[{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Tim","last_name":"Lämmermann","full_name":"Lämmermann, Tim"}],"article_processing_charge":"No","external_id":{"isi":["000535371100002"]},"oa_version":"Published Version","abstract":[{"text":"In contrast to lymph nodes, the lymphoid regions of the spleen—the white pulp—are located deep within the organ, yielding the trafficking paths of T cells in the white pulp largely invisible. In an intravital microscopy tour de force reported in this issue of Immunity, Chauveau et al. show that T cells perform unidirectional, perivascular migration through the enigmatic marginal zone bridging channels. ","lang":"eng"}],"month":"05","intvolume":" 52","scopus_import":"1","main_file_link":[{"open_access":"1","url":"https://pure.mpg.de/pubman/item/item_3265599_2/component/file_3265620/Sixt%20et%20al..pdf"}],"language":[{"iso":"eng"}],"publication_identifier":{"eissn":["10974180"],"issn":["10747613"]},"publication_status":"published","volume":52,"issue":"5","_id":"7876","status":"public","type":"journal_article","article_type":"original","date_updated":"2023-08-21T06:27:18Z","department":[{"_id":"MiSi"}]},{"scopus_import":"1","month":"05","intvolume":" 9","abstract":[{"lang":"eng","text":"Cell migration entails networks and bundles of actin filaments termed lamellipodia and microspikes or filopodia, respectively, as well as focal adhesions, all of which recruit Ena/VASP family members hitherto thought to antagonize efficient cell motility. However, we find these proteins to act as positive regulators of migration in different murine cell lines. CRISPR/Cas9-mediated loss of Ena/VASP proteins reduced lamellipodial actin assembly and perturbed lamellipodial architecture, as evidenced by changed network geometry as well as reduction of filament length and number that was accompanied by abnormal Arp2/3 complex and heterodimeric capping protein accumulation. Loss of Ena/VASP function also abolished the formation of microspikes normally embedded in lamellipodia, but not of filopodia capable of emanating without lamellipodia. Ena/VASP-deficiency also impaired integrin-mediated adhesion accompanied by reduced traction forces exerted through these structures. Our data thus uncover novel Ena/VASP functions of these actin polymerases that are fully consistent with their promotion of cell migration."}],"oa_version":"Published Version","volume":9,"ec_funded":1,"publication_identifier":{"eissn":["2050084X"]},"publication_status":"published","file":[{"file_id":"7914","checksum":"d33bd4441b9a0195718ce1ba5d2c48a6","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"2020_eLife_Damiano_Guercio.pdf","date_created":"2020-06-02T10:35:37Z","creator":"dernst","file_size":10535713,"date_updated":"2020-07-14T12:48:05Z"}],"language":[{"iso":"eng"}],"article_type":"original","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","_id":"7909","file_date_updated":"2020-07-14T12:48:05Z","department":[{"_id":"MiSi"}],"date_updated":"2023-08-21T06:32:25Z","ddc":["570"],"quality_controlled":"1","publisher":"eLife Sciences Publications","oa":1,"doi":"10.7554/eLife.55351","date_published":"2020-05-11T00:00:00Z","date_created":"2020-05-31T22:00:49Z","has_accepted_license":"1","isi":1,"year":"2020","day":"11","publication":"eLife","project":[{"call_identifier":"H2020","_id":"25FE9508-B435-11E9-9278-68D0E5697425","name":"Cellular navigation along spatial gradients","grant_number":"724373"}],"article_number":"e55351","author":[{"first_name":"Julia","last_name":"Damiano-Guercio","full_name":"Damiano-Guercio, Julia"},{"last_name":"Kurzawa","full_name":"Kurzawa, Laëtitia","first_name":"Laëtitia"},{"first_name":"Jan","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D","full_name":"Müller, Jan","last_name":"Müller"},{"first_name":"Georgi A","id":"38C393BE-F248-11E8-B48F-1D18A9856A87","full_name":"Dimchev, Georgi A","orcid":"0000-0001-8370-6161","last_name":"Dimchev"},{"first_name":"Matthias","last_name":"Schaks","full_name":"Schaks, Matthias"},{"first_name":"Maria","id":"34E27F1C-F248-11E8-B48F-1D18A9856A87","full_name":"Nemethova, Maria","last_name":"Nemethova"},{"first_name":"Thomas","last_name":"Pokrant","full_name":"Pokrant, Thomas"},{"last_name":"Brühmann","full_name":"Brühmann, Stefan","first_name":"Stefan"},{"first_name":"Joern","last_name":"Linkner","full_name":"Linkner, Joern"},{"first_name":"Laurent","last_name":"Blanchoin","full_name":"Blanchoin, Laurent"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K"},{"first_name":"Klemens","full_name":"Rottner, Klemens","last_name":"Rottner"},{"first_name":"Jan","full_name":"Faix, Jan","last_name":"Faix"}],"article_processing_charge":"No","external_id":{"isi":["000537208000001"]},"title":"Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion","citation":{"apa":"Damiano-Guercio, J., Kurzawa, L., Müller, J., Dimchev, G. A., Schaks, M., Nemethova, M., … Faix, J. (2020). Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.55351","ama":"Damiano-Guercio J, Kurzawa L, Müller J, et al. Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion. eLife. 2020;9. doi:10.7554/eLife.55351","short":"J. Damiano-Guercio, L. Kurzawa, J. Müller, G.A. Dimchev, M. Schaks, M. Nemethova, T. Pokrant, S. Brühmann, J. Linkner, L. Blanchoin, M.K. Sixt, K. Rottner, J. Faix, ELife 9 (2020).","ieee":"J. Damiano-Guercio et al., “Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion,” eLife, vol. 9. eLife Sciences Publications, 2020.","mla":"Damiano-Guercio, Julia, et al. “Loss of Ena/VASP Interferes with Lamellipodium Architecture, Motility and Integrin-Dependent Adhesion.” ELife, vol. 9, e55351, eLife Sciences Publications, 2020, doi:10.7554/eLife.55351.","ista":"Damiano-Guercio J, Kurzawa L, Müller J, Dimchev GA, Schaks M, Nemethova M, Pokrant T, Brühmann S, Linkner J, Blanchoin L, Sixt MK, Rottner K, Faix J. 2020. Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion. eLife. 9, e55351.","chicago":"Damiano-Guercio, Julia, Laëtitia Kurzawa, Jan Müller, Georgi A Dimchev, Matthias Schaks, Maria Nemethova, Thomas Pokrant, et al. “Loss of Ena/VASP Interferes with Lamellipodium Architecture, Motility and Integrin-Dependent Adhesion.” ELife. eLife Sciences Publications, 2020. https://doi.org/10.7554/eLife.55351."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8"},{"date_updated":"2023-08-22T07:56:04Z","department":[{"_id":"MiSi"}],"_id":"8132","status":"public","type":"journal_article","article_type":"original","language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"eissn":["24709468"]},"volume":5,"issue":"49","oa_version":"None","pmid":1,"abstract":[{"text":"The WAVE regulatory complex (WRC) is crucial for assembly of the peripheral branched actin network constituting one of the main drivers of eukaryotic cell migration. Here, we uncover an essential role of the hematopoietic-specific WRC component HEM1 for immune cell development. Germline-encoded HEM1 deficiency underlies an inborn error of immunity with systemic autoimmunity, at cellular level marked by WRC destabilization, reduced filamentous actin, and failure to assemble lamellipodia. Hem1−/− mice display systemic autoimmunity, phenocopying the human disease. In the absence of Hem1, B cells become deprived of extracellular stimuli necessary to maintain the strength of B cell receptor signaling at a level permissive for survival of non-autoreactive B cells. This shifts the balance of B cell fate choices toward autoreactive B cells and thus autoimmunity.","lang":"eng"}],"intvolume":" 5","month":"07","scopus_import":"1","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ieee":"E. Salzer et al., “The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity,” Science Immunology, vol. 5, no. 49. AAAS, 2020.","short":"E. Salzer, S. Zoghi, M.G. Kiss, F. Kage, C. Rashkova, S. Stahnke, M. Haimel, R. Platzer, M. Caldera, R.C. Ardy, B. Hoeger, J. Block, D. Medgyesi, C. Sin, S. Shahkarami, R. Kain, V. Ziaee, P. Hammerl, C. Bock, J. Menche, L. Dupré, J.B. Huppa, M.K. Sixt, A. Lomakin, K. Rottner, C.J. Binder, T.E.B. Stradal, N. Rezaei, K. Boztug, Science Immunology 5 (2020).","ama":"Salzer E, Zoghi S, Kiss MG, et al. The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity. Science Immunology. 2020;5(49). doi:10.1126/sciimmunol.abc3979","apa":"Salzer, E., Zoghi, S., Kiss, M. G., Kage, F., Rashkova, C., Stahnke, S., … Boztug, K. (2020). The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity. Science Immunology. AAAS. https://doi.org/10.1126/sciimmunol.abc3979","mla":"Salzer, Elisabeth, et al. “The Cytoskeletal Regulator HEM1 Governs B Cell Development and Prevents Autoimmunity.” Science Immunology, vol. 5, no. 49, eabc3979, AAAS, 2020, doi:10.1126/sciimmunol.abc3979.","ista":"Salzer E, Zoghi S, Kiss MG, Kage F, Rashkova C, Stahnke S, Haimel M, Platzer R, Caldera M, Ardy RC, Hoeger B, Block J, Medgyesi D, Sin C, Shahkarami S, Kain R, Ziaee V, Hammerl P, Bock C, Menche J, Dupré L, Huppa JB, Sixt MK, Lomakin A, Rottner K, Binder CJ, Stradal TEB, Rezaei N, Boztug K. 2020. The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity. Science Immunology. 5(49), eabc3979.","chicago":"Salzer, Elisabeth, Samaneh Zoghi, Máté G. Kiss, Frieda Kage, Christina Rashkova, Stephanie Stahnke, Matthias Haimel, et al. “The Cytoskeletal Regulator HEM1 Governs B Cell Development and Prevents Autoimmunity.” Science Immunology. AAAS, 2020. https://doi.org/10.1126/sciimmunol.abc3979."},"title":"The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity","external_id":{"pmid":["32646852"],"isi":["000546994600004"]},"article_processing_charge":"No","author":[{"full_name":"Salzer, Elisabeth","last_name":"Salzer","first_name":"Elisabeth"},{"first_name":"Samaneh","last_name":"Zoghi","full_name":"Zoghi, Samaneh"},{"last_name":"Kiss","full_name":"Kiss, Máté G.","first_name":"Máté G."},{"first_name":"Frieda","full_name":"Kage, Frieda","last_name":"Kage"},{"last_name":"Rashkova","full_name":"Rashkova, Christina","first_name":"Christina"},{"full_name":"Stahnke, Stephanie","last_name":"Stahnke","first_name":"Stephanie"},{"first_name":"Matthias","last_name":"Haimel","full_name":"Haimel, Matthias"},{"full_name":"Platzer, René","last_name":"Platzer","first_name":"René"},{"full_name":"Caldera, Michael","last_name":"Caldera","first_name":"Michael"},{"first_name":"Rico Chandra","full_name":"Ardy, Rico Chandra","last_name":"Ardy"},{"full_name":"Hoeger, Birgit","last_name":"Hoeger","first_name":"Birgit"},{"first_name":"Jana","last_name":"Block","full_name":"Block, Jana"},{"last_name":"Medgyesi","full_name":"Medgyesi, David","first_name":"David"},{"first_name":"Celine","full_name":"Sin, Celine","last_name":"Sin"},{"last_name":"Shahkarami","full_name":"Shahkarami, Sepideh","first_name":"Sepideh"},{"last_name":"Kain","full_name":"Kain, Renate","first_name":"Renate"},{"full_name":"Ziaee, Vahid","last_name":"Ziaee","first_name":"Vahid"},{"full_name":"Hammerl, Peter","last_name":"Hammerl","first_name":"Peter"},{"first_name":"Christoph","full_name":"Bock, Christoph","last_name":"Bock"},{"last_name":"Menche","full_name":"Menche, Jörg","first_name":"Jörg"},{"first_name":"Loïc","last_name":"Dupré","full_name":"Dupré, Loïc"},{"last_name":"Huppa","full_name":"Huppa, Johannes B.","first_name":"Johannes B."},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Lomakin, Alexis","last_name":"Lomakin","first_name":"Alexis"},{"last_name":"Rottner","full_name":"Rottner, Klemens","first_name":"Klemens"},{"first_name":"Christoph J.","full_name":"Binder, Christoph J.","last_name":"Binder"},{"first_name":"Theresia E.B.","last_name":"Stradal","full_name":"Stradal, Theresia E.B."},{"first_name":"Nima","full_name":"Rezaei, Nima","last_name":"Rezaei"},{"first_name":"Kaan","last_name":"Boztug","full_name":"Boztug, Kaan"}],"article_number":"eabc3979","publication":"Science Immunology","day":"10","year":"2020","isi":1,"date_created":"2020-07-19T22:00:58Z","date_published":"2020-07-10T00:00:00Z","doi":"10.1126/sciimmunol.abc3979","publisher":"AAAS","quality_controlled":"1"}]