共查询到20条相似文献,搜索用时 15 毫秒
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PRL activates the cyclin D1 promoter via the Jak2/Stat pathway 总被引:12,自引:0,他引:12
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Hou Z Srivastava S Mistry MJ Herbst MP Bailey JP Horseman ND 《Molecular endocrinology (Baltimore, Md.)》2003,17(10):1910-1920
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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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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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Receptor activator of NF-kappaB ligand regulates the proliferation of mammary epithelial cells via Id2 下载免费PDF全文
Kim NS Kim HJ Koo BK Kwon MC Kim YW Cho Y Yokota Y Penninger JM Kong YY 《Molecular and cellular biology》2006,26(3):1002-1013
Receptor activator of NF-kappaB ligand (RANKL) is a key regulator for mammary gland development during pregnancy. RANKL-deficient mice display impaired development of lobulo-alveolar mammary structures. Similar mammary gland defects have been reported in mice lacking Id2. Here we report that RANKL induces the proliferation of mammary epithelial cells via Id2. RANKL triggers marked nuclear translocation of Id2 in mammary epithelial cells. In vivo studies further demonstrated the defective nuclear translocation of Id2, but the normal expression of cyclin D1, in the mammary epithelial cells of rankl-/- mice. In vitro studies with nuclear localization sequence-tagged Id2 revealed that the nuclear localization of Id2 itself is critical for the downregulation of p21 promoter activity. Moreover, RANKL stimulation failed to induce cell growth and to downregulate p21 expression in Id2-/- mammary epithelial cells. Our results indicate that the inhibitor of helix-loop-helix protein, Id2, is critical to control the proliferation of mammary epithelial cells in response to RANKL stimulation. 相似文献
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Neilson LM Zhu J Xie J Malabarba MG Sakamoto K Wagner KU Kirken RA Rui H 《Molecular endocrinology (Baltimore, Md.)》2007,21(9):2218-2232
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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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