Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 배윤수 | * |
dc.date.accessioned | 2017-02-15T08:02:44Z | - |
dc.date.available | 2017-02-15T08:02:44Z | - |
dc.date.issued | 2006 | * |
dc.identifier.issn | 1465-7392 | * |
dc.identifier.other | OAK-3686 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/234171 | - |
dc.description.abstract | Growth hormone binds to its membrane receptor (GHR), whereby it regulates many cellular functions, including proliferation, differentiation and chemotaxis. However, although the activation of growth hormone-mediated signalling is well understood, the precise mechanism responsible for its regulation has not been elucidated. Here, we demonstrate that phospholipase Cγ1 (PLCγ1) modulates the action of growth hormone-mediated signalling by interacting with tyrosine kinase Jak2 (janus kinase 2) in a growth hormone-dependent manner. In the absence of PLCγ1 (PLCγ1-/-), growth hormone-induced JAK2 and STAT5 phosphorylation significantly increased in mouse embryonic fibroblasts (MEFs). Furthermore, the re-expression of PLCγ1 reduced growth hormone-induced Jak2 activation. Growth hormone-induced Jak2 phosphorylation was enhanced by siRNA-specific knockdown of PLCγ1. Interestingly, PLCγ1 physically linked Jak2 and protein tyrosine phosphatase-1B (PTP-1B) by binding to both using different domains, and this process was implicated in the modulation of cytokine signalling through Jak2. In addition, in PLCγ1-/- MEFs, growth hormone-dependent c-Fos activation was upregulated and growth hormone-induced proliferation was potentiated. These results suggest that PLCγ1 has a key function in the regulation of growth hormone-mediated signalling by negatively regulating Jak2 activation. | * |
dc.language | English | * |
dc.title | Phospholipase Cγ1 negatively regulates growth hormone signalling by forming a ternary complex with Jak2 and protein tyrosine phosphatase-1B | * |
dc.type | Article | * |
dc.relation.issue | 12 | * |
dc.relation.volume | 8 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 1389 | * |
dc.relation.lastpage | 1397 | * |
dc.relation.journaltitle | Nature Cell Biology | * |
dc.identifier.doi | 10.1038/ncb1509 | * |
dc.identifier.wosid | WOS:000242419800015 | * |
dc.identifier.scopusid | 2-s2.0-33751536492 | * |
dc.author.google | Choi J.H. | * |
dc.author.google | Kim H.S. | * |
dc.author.google | Kim S.-H. | * |
dc.author.google | Yang Y.R. | * |
dc.author.google | Bae Y.S. | * |
dc.author.google | Chang J.-S. | * |
dc.author.google | Moo Kwon H. | * |
dc.author.google | Ryu S.H. | * |
dc.author.google | Suh P.-G. | * |
dc.contributor.scopusid | 배윤수(15031067200) | * |
dc.date.modifydate | 20240415133331 | * |