Show simple item record Csépányi-Kömi, Roland Wisniewski, Éva Bartos, Balázs Ádám Levai P Németh, Tamás Balázs, Bernadett Kurz AR Bierschenk S Sperandio M Ligeti, Erzsébet 2018-03-13T10:02:12Z 2018-03-13T10:02:12Z 2016
dc.identifier.citation pagination=2807-2815; journalVolume=197; journalIssueNumber=7; journalTitle=JOURNAL OF IMMUNOLOGY;
dc.identifier.uri doi:10.4049/jimmunol.1502342
dc.description.abstract ARHGAP25 is a Rac-specific GTPase-activating protein that is expressed primarily in hematopoietic cells. The involvement of ARHGAP25 in regulating the recruitment of leukocytes to inflammatory sites was investigated in genetically modified mice. Using intravital microscopy, we show that Arhgap25 deficiency affects all steps of leukocyte recruitment with a predominant enhancement of transendothelial migration of neutrophilic granulocytes. Increased transmigration of Arhgap25-deficient leukocytes is demonstrated in inflamed cremaster muscle venules, in a peritonitis model, and in an in vitro chemotaxis assay. Using bone marrow chimeric mice lacking ARHGAP25 in the hematopoietic compartment, we show that enhanced migration in the absence of ARHGAP25 is due to defective leukocyte function. In search for potential mechanisms of ARHGAP25-regulated migration of neutrophils, we detected an increase in the amount of active, GTP-bound Rac and Rac-dependent cytoskeletal changes in the absence of ARHGAP25, suggesting a critical role of ARHGAP25 in counterbalancing the Rac-activating effect of nucleotide exchange factors. Taken together, using Arhgap25-deficient mice, we identified ARHGAP25 as a relevant negative regulator of leukocyte transendothelial migration.
dc.relation.ispartof urn:issn:0022-1767
dc.title Rac GTPase Activating Protein ARHGAP25 Regulates Leukocyte Transendothelial Migration in Mice.
dc.type Journal Article 2018-02-16T14:24:09Z
dc.language.rfc3066 en
dc.identifier.mtmt 3105029
dc.identifier.wos 000385004600030
dc.identifier.scopus 84989815268
dc.identifier.pubmed 27566826
dc.contributor.department SE/AOK/I/Élettani Intézet
dc.contributor.institution Semmelweis Egyetem
dc.mtmt.swordnote R.C.-K. and E.W. contributed equally to this work. M.S. and E.L. contributed equally to this work.

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