http://purl.uniprot.org/citations/17620366 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/17620366 | http://www.w3.org/2000/01/rdf-schema#comment | "Acute renal failure due to ischemia/reperfusion involves disruption of integrin-mediated cellular adhesion and activation of the extracellular signal-regulated kinase (ERK) pathway. The dynamics of focal adhesion organization and phosphorylation during ischemia/reperfusion in relation to ERK activation are unknown. In control kidneys, protein tyrosine-rich focal adhesions, containing focal adhesion kinase, paxillin, and talin, were present at the basolateral membrane of tubular cells and colocalized with short F-actin stress fibers. Unilateral renal ischemia/reperfusion caused a reversible protein dephosphorylation and loss of focal adhesions. The focal adhesion protein phosphorylation rebounded in a biphasic manner, in association with increased focal adhesion kinase, Src, and paxillin tyrosine phosphorylation. Preceding phosphorylation of these focal adhesion proteins, reperfusion caused increased phosphorylation of ERK. The specific mitogen-activated protein kinase kinase 1/2 inhibitor U0126 prevented ERK activation and attenuated focal adhesion kinase, paxillin, and Src phosphorylation, focal adhesion restructuring, and ischemia/reperfusion-induced renal injury. We propose a model whereby ERK activation enhanced protein tyrosine phosphorylation during ischemia/reperfusion, thereby driving the dynamic dissolution and restructuring of focal adhesions and F-actin cytoskeleton during reperfusion and renal injury."xsd:string |
http://purl.uniprot.org/citations/17620366 | http://purl.org/dc/terms/identifier | "doi:10.2353/ajpath.2007.060805"xsd:string |
http://purl.uniprot.org/citations/17620366 | http://purl.uniprot.org/core/author | "de Graauw M."xsd:string |
http://purl.uniprot.org/citations/17620366 | http://purl.uniprot.org/core/author | "Qin Y."xsd:string |
http://purl.uniprot.org/citations/17620366 | http://purl.uniprot.org/core/author | "van de Water B."xsd:string |
http://purl.uniprot.org/citations/17620366 | http://purl.uniprot.org/core/author | "Pont C."xsd:string |
http://purl.uniprot.org/citations/17620366 | http://purl.uniprot.org/core/author | "van Buren L."xsd:string |
http://purl.uniprot.org/citations/17620366 | http://purl.uniprot.org/core/author | "Alderliesten M."xsd:string |
http://purl.uniprot.org/citations/17620366 | http://purl.uniprot.org/core/author | "Oldenampsen J."xsd:string |
http://purl.uniprot.org/citations/17620366 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
http://purl.uniprot.org/citations/17620366 | http://purl.uniprot.org/core/name | "Am J Pathol"xsd:string |
http://purl.uniprot.org/citations/17620366 | http://purl.uniprot.org/core/pages | "452-462"xsd:string |
http://purl.uniprot.org/citations/17620366 | http://purl.uniprot.org/core/title | "Extracellular signal-regulated kinase activation during renal ischemia/reperfusion mediates focal adhesion dissolution and renal injury."xsd:string |
http://purl.uniprot.org/citations/17620366 | http://purl.uniprot.org/core/volume | "171"xsd:string |
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