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INS — STAT5A

Text-mined interactions from Literome

Storz et al., FEBS Lett 1999 (Rhabdomyosarcoma) : Insulin selectively activates STAT5b, but not STAT5a , via a JAK2 independent signalling pathway in Kym-1 rhabdomyosarcoma cells
Sadowski et al., J Biol Chem 2001 : We can recapitulate robust insulin activation of Stat5 in C2C12 cells by stable overexpression of the human IR (hIR) ... To identify insulin activated genes that are Stat5 targets, we also overexpressed an IR mutant ( LA-hIR ) that signals normally for mitogen activated protein kinase- and phosphatidylinositol 3-kinase dependent pathways but is deficient in Stat5 signaling in response to insulin ... Therefore, our results suggest that insulin induction of SOCS-2, and in part SOCS-3 mRNA expression, is mediated by Stat5 and can be independent of mitogen activated protein kinase and phosphatidylinositol 3-kinase signaling pathways
Le et al., Mol Endocrinol 2002 (Liver Neoplasms, Experimental) : In coimmunoprecipitation assays, insulin stimulated Stat5 activation correlates with Stat5 recruitment to the IR ... Expression of dominant negative ( DN ) JAKs, the JAK inhibitor suppressor of cytokine signaling 1, or pretreatment with the JAK inhibitor, AG490, reduces, but does not eliminate, insulin induced Stat5 activation ... Expression of the appropriate pair of DN JAKs in each of the singly JAK-deficient cell lines further establishes a component of insulin stimulated Stat5 activation that is JAK independent ... Increasing the concentration of Stat5 proteins in cells favors the direct phosphorylation of Stat5 by the IR kinase where the DN-JAK inhibition of insulin stimulated Stat5 activation becomes insignificant ... At physiological levels of Stat5 however, we propose that JAKs and the IR both contribute to the insulin induced phosphorylation of Stat5
Zvonic et al., Biochem Biophys Res Commun 2003 : In our studies, we have shown that physiological levels of insulin do not induce STAT 5 tyrosine phosphorylation or affect the nuclear distribution of STATs 5A or 5B in 3T3-L1 adipocytes
Story et al., Obesity (Silver Spring) 2006 : However, INS did not block the GH-induced activation of STAT5 , and GH did not block the INS induction of ERK activity or of increased glucose uptake
Nielsen et al., J Clin Endocrinol Metab 2008 : In muscle, ERK1/2 phosphorylation was increased by insulin , but insulin per se did not induce phosphorylation of Stat5
Menzies et al., Funct Integr Genomics 2010 : Subsequent experiments in HCll cells confirmed that Stat5a and Elf5 gene expression could be induced in the absence of prolactin but in the presence of insulin
Zhang et al., Lipids in health and disease 2013 : Effects of insulin and IGF-I on growth hormone- induced STAT5 activation in 3T3-F442A adipocytes ... Insulin alone did not induce STAT5 tyrosine phosphorylation, but enhanced GH-induced STAT5 activation ... These results indicate that both insulin and IGF-I specifically potentiated GH mediated STAT5 activation in mature adipose cells
Chen et al., Proc Natl Acad Sci U S A 1997 : Insulin stimulates tyrosine phosphorylation of overexpressed Stat5b-Ct and endogenous Stat5 in cells overexpressing IR
Storz et al., FEBS Lett 1998 : TNF downregulated insulin induced insulin receptor kinase activity and insulin induced activation of the transcription factor STAT5