Gene interactions and pathways from curated databases and text-mining

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IRS1 — SLC2A4

Text-mined interactions from Literome

Zhou et al., Mol Endocrinol 1999 : Overexpression of IRS-1 led to a 2-fold increase in cell surface GLUT4-HA in cells incubated in the absence of insulin ; overexpression of either IRS-3 or IRS-4 elicited a larger increase in cell surface GLUT4-HA
Ishizuka et al., Diabetes 1999 (Diabetes, Gestational...) : Overexpression of GLUT4 in db/+TG6 mice markedly improved glucose stimulated insulin secretion, by 250 %, and increased IRbeta, IRS-1 , and p85alpha phosphorylation twofold, despite no change in concentration of these proteins
Huang et al., J Biol Chem 2005 : We conclude that insulin stimulated Akt1 phosphorylation, actin remodeling, GLUT4 translocation, and glucose uptake are regulated mainly by IRS-1 , whereas IRS-2 contributes selectively to ERK signaling, and Akt2 and p38MAPK lie downstream of both IRS in muscle cells
Viscarra et al., Am J Physiol Regul Integr Comp Physiol 2011 (Insulin Resistance) : Glut4 increased ( 31 % ) with fasting despite the significant decreases in the cellular content of phosphatidylinositol 3-kinase as well as phosphorylated insulin receptor, insulin receptor substrate-1 , and Akt2
Manna et al., J Biol Chem 2011 : Treatment with LC, H ( 2 ) S, or PIP3 increased the phosphorylation of IRS1 , AKT, and PKC?/? as well as GLUT4 activation and glucose utilization in HG-treated cells
Quon et al., J Biol Chem 1994 : Insulin receptor substrate 1 mediates the stimulatory effect of insulin on GLUT4 translocation in transfected rat adipose cells ... Overexpression of human IRS-1 increased the basal cell surface GLUT4 to nearly the maximal level in the absence of insulin
Kaburagi et al., J Biol Chem 1997 : Role of insulin receptor substrate-1 and pp60 in the regulation of insulin induced glucose transport and GLUT4 translocation in primary adipocytes
Zhou et al., J Biol Chem 1997 : Overexpression of IRS-1 or IRS-2 in adipose cells resulted in a significant increase in the basal level of cell surface GLUT4 ( in the absence of insulin )
Anai et al., Diabetes 1999 (Insulin Resistance) : Insulin receptor substrate (IRS)-1 and IRS-2, which mediate phosphatidylinositol (PI) 3-kinase activation, play essential roles in insulin induced translocation of GLUT4 and in glycogen synthesis