共查询到20条相似文献,搜索用时 656 毫秒
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J Frasor U Barkai L Zhong A T Fazleabas G Gibori 《Molecular endocrinology (Baltimore, Md.)》2001,15(11):1941-1952
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ErbB receptor-induced activation of stat transcription factors is mediated by Src tyrosine kinases. 总被引:16,自引:0,他引:16
M A Olayioye I Beuvink K Horsch J M Daly N E Hynes 《The Journal of biological chemistry》1999,274(24):17209-17218
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Progestins induce transcriptional activation of signal transducer and activator of transcription 3 (Stat3) via a Jak- and Src-dependent mechanism in breast cancer cells 下载免费PDF全文
Proietti C Salatino M Rosemblit C Carnevale R Pecci A Kornblihtt AR Molinolo AA Frahm I Charreau EH Schillaci R Elizalde PV 《Molecular and cellular biology》2005,25(12):4826-4840
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José Manuel García-Martínez Annarica Calcabrini Lorena González Esther Martín-Forero María Teresa Agulló-Ortuño Valérie Simon Harriet Watkin Steve M. Anderson Serge Roche Jorge Martín-Pérez 《Cellular signalling》2010,22(3):415-426
The cytokine prolactin (PRL) plays important roles in the proliferation and differentiation of the mammary gland and it has been implicated in tumorigenesis. The prolactin receptor (PRLR) is devoid of catalytic activity and its mitogenic response is controlled by cytoplasmic tyrosine kinases of the Src (SFK) and Jak families. How PRLR uses these kinases for signaling is not well understood. Previous studies indicated that PRLR-induced Jak2 activation does not require SFK catalytic activity in favor of separate signaling operating on this cellular response. Here we show that, nevertheless, PRLR requires Src-SH2 and -SH3 domains for Jak2 signaling. In W53 lymphoid cells, conditional expression of two c-Src non-catalytic mutants, either SrcK295M/Y527F or Src?K, whose SH3 and SH2 domains are exposed, controls Jak2/Stat5 activation by recruiting Jak2, avoiding its activation by endogenous active SFK. In contrast, the kinase inactive SrcK295M mutant, with inaccessible SH3 and SH2 domains, does not. Furthermore, all three mutants attenuate PRLR-induced Akt and p70S6K activation. Accordingly, PRLR-induced Jak2/Stat5 signaling is inhibited in MCF7 breast cancer cells by Src depletion, expression of SrcK295M/Y527F or active Src harboring an inactive SH2 (SrcR175L) or SH3 domain (SrcW118A). Finally, Jak2/Stat5 pathway is also reduced in Src?/? mice mammary glands. We thus conclude that, in addition to Akt and p70S6K, SFK regulate PRLR-induced Jak2 signaling through a kinase-independent mechanism. 相似文献
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Regulation of Stat3 activation by MEK kinase 1 总被引:6,自引:0,他引:6
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