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dc.contributor.author Lőrincz, Márton Ákos
dc.contributor.author Szarvas G
dc.contributor.author Smith SME
dc.contributor.author Ligeti, Erzsébet
dc.date.accessioned 2016-10-13T09:44:50Z
dc.date.available 2016-10-13T09:44:50Z
dc.date.issued 2014
dc.identifier 84890920958
dc.identifier.citation pagination=65-71; journalVolume=68; journalTitle=FREE RADICAL BIOLOGY AND MEDICINE;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/2706
dc.identifier.uri doi:10.1016/j.freeradbiomed.2013.12.001
dc.description.abstract Precise spatiotemporal regulation of O2 --generating NADPH oxidases (Nox) is a vital requirement. In the case of Nox1-3, which depend on the small GTPase Rac, acceleration of GTP hydrolysis by GTPase activating protein (GAP) could represent a feasible temporal control mechanism. Our goal was to investigate the molecular interactions between RacGAPs and phagocytic Nox2 in neutrophilic granulocytes. In structural studies we revealed that simultaneous interaction of Rac with its effector protein p67phox and regulatory protein RacGAP was sterically possible. The effect of RacGAPs was experimentally investigated in a cell-free O2 --generating system consisting of isolated membranes and recombinant p47phox and p67phox proteins. Addition of soluble RacGAPs decreased O 2 - production and there was no difference in the effect of four RacGAPs previously identified in neutrophils. Depletion of membrane-associated RacGAPs had a selective effect: a decrease in ARHGAP1 or ARHGAP25 level increased O2 - production but a depletion of ARHGAP35 had no effect. Only membrane-localized RacGAPs seem to be able to interact with Rac when it is assembled in the Nox2 complex. Thus, in neutrophils multiple RacGAPs are involved in the control of O2 - production by Nox2, allowing selective regulation via different signaling pathways. © 2013 Elsevier Inc.
dc.relation.ispartof urn:issn:0891-5849
dc.title Role of Rac GTPase activating proteins in regulation of NADPH oxidase in human neutrophils
dc.type Journal Article
dc.date.updated 2015-11-25T10:14:46Z
dc.language.rfc3066 en
dc.identifier.mtmt 2497073
dc.identifier.wos 000332429900007
dc.identifier.pubmed 24321316
dc.contributor.department SE/AOK/I/Élettani Intézet
dc.contributor.institution Semmelweis Egyetem


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