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dc.contributor.authorJiang, Hongyanen_US
dc.contributor.authorSha, Su-Huaen_US
dc.contributor.authorSchacht, Jochenen_US
dc.date.accessioned2007-01-17T15:54:23Z
dc.date.available2007-01-17T15:54:23Z
dc.date.issued2006en_US
dc.identifier.citationJiang, Hongyan; Sha, Su-Hua; Schacht, Jochen (2006)."Rac/Rho pathway regulates actin depolymerization induced by aminoglycoside antibiotics." Journal of Neuroscience Research 9999(9999): NA-NA. <http://hdl.handle.net/2027.42/49295>en_US
dc.identifier.issn0360-4012en_US
dc.identifier.issn1097-4547en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/49295
dc.description.abstractStress stimuli can lead to remodeling of the actin cytoskeleton and subsequent alteration of cell adhesion and permeation as well as cell functions and cell fate. We investigated redox-dependent Rho GTPase-linked pathways controlling the actin cytoskeleton in the inner ear of the CBA mouse, by using aminoglycoside antibiotics as a noxious stimulus that causes loss of sensory cells via the formation of reactive oxygen species. Kanamycin treatment in vivo interfered with the formation of F-actin, disturbed the arrangement of Β-actin in the stereocilia of outer hair cells, and altered the intermittent adherens junction/tight junction complexes between outer hair cells and supporting cells. The drug treatment also activated Rac1 and promoted the formation of the complex of Rac1 and p67phox while decreasing the activity of RhoA and reducing the formation of the RhoA/p140mDia complex. In inner-ear-derived cell lines, expression of mutated Rac1 changed the structural arrangement of F-actin and diminished the immunoreactivity of p140mDia. These findings suggest that actin depolymerization induced by kanamycin is mediated by Rac1 activation, followed by the formation of superoxide by NADPH oxidase. These changes will ultimately contribute to aminoglycoside-induced loss of hair cells. © 2006 Wiley-Liss, Inc.en_US
dc.format.extent367487 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherNeuroscience, Neurology and Psychiatryen_US
dc.titleRac/Rho pathway regulates actin depolymerization induced by aminoglycoside antibioticsen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbsecondlevelPsychologyen_US
dc.subject.hlbsecondlevelPublic Healthen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.subject.hlbtoplevelSocial Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumKresge Hearing Research Institute, Department of Otolaryngology, University of Michigan, Ann Arbor, Michigan ; This first two authors contributed equally to this work.en_US
dc.contributor.affiliationumKresge Hearing Research Institute, Department of Otolaryngology, University of Michigan, Ann Arbor, Michiganen_US
dc.contributor.affiliationumKresge Hearing Research Institute, Department of Otolaryngology, University of Michigan, Ann Arbor, Michigan ; Kresge Hearing Research Institute, Department of Otolaryngology, University of Michigan, Ann Arbor, MI 48109-0506en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/49295/1/2535_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/jnr.20833en_US
dc.identifier.sourceJournal of Neuroscience Researchen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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