Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 허규정 | * |
dc.contributor.author | 배윤수 | * |
dc.date.accessioned | 2016-08-28T11:08:24Z | - |
dc.date.available | 2016-08-28T11:08:24Z | - |
dc.date.issued | 2000 | * |
dc.identifier.issn | 0021-9258 | * |
dc.identifier.other | OAK-404 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/218625 | - |
dc.description.abstract | Autophosphorylation of the platelet-derived growth factor (PDGF) receptor triggers intracellular signaling cascades as a result of recruitment of Src homology 2 domain-containing enzymes, including phosphatidyl-inositol 3-kinase (PI3K), the GTPase-activating protein of Ras (GAP), the protein- tyrosine phosphatase SHP-2, and phospholipase C-γ1 (PLC-γ1), to specific phosphotyrosine residues. The roles of these various effectors in PDGF- induced generation of H2O2 have now been investigated in HepG2 cells expressing various PDGF receptor mutants. These mutants included a kinase- deficient receptor and receptors in which various combinations of the tyrosine residues required for the binding of PI3K (Tyr740 and Tyr751), GAP (Tyr771), SHP-2 (Tyr1009), or PLC-γ1 (Tyr1021) were mutated to Phe. PDGF failed to increase H2O2 production in cells expressing either the kinase-deficient mutant or a receptor in which the two Tyr residues required for the binding of PI3K were re- placed by Phe. In contrast, PDGF- induced H2O2 production in cells expressing a receptor in which the binding sites for GAP, SHP-2, and PLC-γ1 were all mutated was slightly greater than that in cells expressing the wild-type receptor. Only the PI3K binding site was alone sufficient for PDGF-induced H2O2 production. The effect of PDGF on H2O2 generation was blocked by the PI3K inhibitors LY294002 and wortmannin or by overexpression of a dominant negative mutant of Rac1. These results suggest that a product of PI3K is required for PDGF-induced production of H2O2 in nonphagocytic cells, and that Rac1 mediates signaling between the PI3K product and the putative NADPH oxidase. | * |
dc.language | English | * |
dc.title | Platelet-derived growth factor-induced H2O2 production requires the activation of phosphatidylinositol 3-kinase | * |
dc.type | Article | * |
dc.relation.issue | 14 | * |
dc.relation.volume | 275 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 10527 | * |
dc.relation.lastpage | 10531 | * |
dc.relation.journaltitle | Journal of Biological Chemistry | * |
dc.identifier.doi | 10.1074/jbc.275.14.10527 | * |
dc.identifier.wosid | WOS:000086345600086 | * |
dc.identifier.scopusid | 2-s2.0-0001288948 | * |
dc.author.google | Bae Y.S. | * |
dc.author.google | Sung J.-Y. | * |
dc.author.google | Kim O.-S. | * |
dc.author.google | Kim Y.J. | * |
dc.author.google | Hur K.C. | * |
dc.author.google | Kazlauskas A. | * |
dc.author.google | Rhee S.G. | * |
dc.contributor.scopusid | 허규정(7005230301) | * |
dc.contributor.scopusid | 배윤수(15031067200) | * |
dc.date.modifydate | 20240415133331 | * |