Gene interactions and pathways from curated databases and text-mining

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GRB2 — INS

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Wada et al., Endocrinology 1999 : Insulin stimulation of Shc association with Grb2 , which is important for p21ras-MAP kinase activation, was decreased by overexpression of WT- and 2F-SHIP ... Importantly, insulin induced Shc x Grb2 association was not detectably reduced in deltaSH2-SHIP cells
Tsakiridis et al., Microsc Res Tech 1999 : Intact actin filaments appear to be essential for mediation of early events such as association of Shc with Grb2 in response to insulin , which leads to stimulation of gene expression
Uchida et al., Mol Cell Biol 2000 : Insulin promoted the association of Grb-2 with IRS-1 and IRS-4, whereas IRS-2 weakly bound Grb-2 ; consequently, IRS-1 and IRS-4 enhanced insulin stimulated mitogen activated protein kinase activity
Nakajima et al., J Biol Chem 2000 (Carcinoma, Hepatocellular) : In contrast, insulin induced association of Shc and Grb2 was not inhibited
Xu et al., Biochemistry 2000 : Insulin gene transcription was stimulated by insulin receptor signaling and insulin mimetic compound ( L-783 281 ) in a glucose- and Grb2 dependent manner
Valverde et al., Mol Cell Biol 2001 : Association of insulin receptor substrate 1 (IRS-1) y895 with Grb-2 mediates the insulin signaling involved in IRS-1-deficient brown adipocyte mitogenesis ... Reconstitution of IRS-1-deficient brown adipocytes with wild-type IRS-1 restored insulin induced IRS-1 and SHC tyrosine phosphorylation and IRS-1-Grb-2 , IRS-1-SHC, and SHC-Grb-2 associations, leading to the activation of MAPK and enhancement of DNA synthesis
Mur et al., Diabetes 2002 : However, SHC expression and SHC tyrosine phosphorylation and its association with Grb-2 were unaltered in response to insulin in IGF-IR -- deficient brown adipocytes
Sano et al., J Biol Chem 2002 : The results from the overexpression of IRAS, where its amount was about the same as that of IRS-4, indicated that IRAS associated directly with IRS-4 and showed that the increased complexation of IRS-4 with IRAS did not alter the insulin stimulated tyrosine phosphorylation of IRS-4 or the association of IRS-4 with phosphatidylinositol 3-kinase or Grb2
Lee et al., J Biol Chem 2003 : Insulin stimulation of JNK activity required phosphatidylinositol 3-kinase and Grb2 signaling
Arribas et al., J Biol Chem 2003 : However, although insulin promoted the association of Grb-2 with recombinant IRS-3 in IRS-1-/- cells, the exogenous expression of this IRS family member failed to activate p42/44 MAPK and mitogenesis in brown adipocytes lacking IRS-1
Biedi et al., Endocrinology 2003 : Here we show that insulin also induces Shc phosphorylation and Grb2 recruitment to caveolae, but with a significantly different time course compared with IGF-I
Liu et al., Am J Physiol Endocrinol Metab 2009 (Insulin Resistance) : Suppressing Grb2 expression in C ( 2 ) C ( 12 ) myoblasts enhances insulin stimulated insulin receptor substrate (IRS)-1 , tyrosine phosphorylation, and Akt phosphorylation, which is associated with decreased IRS-1 serine phosphorylation at residues 307, 612, and 636/639
Cherniack et al., J Biol Chem 1995 : Immunoblot analysis of these precipitates revealed that insulin causes a marked hyperphosphorylation of Sos1 and a 50 % decrease in Grb2 associated with Sos proteins under these conditions
Yamauchi et al., Mol Cell Biol 1994 : Further, expression of Grb2 in parental CHO cells had no effect on insulin signaling, whereas Grb2 increased insulin activation of reporter gene expression in CHO/IR cells ... To assess the relative effects of various insulin receptor, IRS1, and Grb2 levels on insulin signaling, parental CHO cells were transiently transfected with various combinations of expression plasmids encoding these proteins
Pronk et al., Mol Cell Biol 1994 : From these results, we conclude that after insulin and EGF treatment, Shc associates with both Grb2 and mSOS and therefore may mediate , at least in part, insulin- and EGF induced activation of p21ras
Myers et al., Mol Cell Biol 1994 : Role of IRS-1-GRB-2 complexes in insulin signaling
Ohmichi et al., J Biol Chem 1994 : NGF and EGF also induced the association of Shc proteins with a Grb2 fusion protein or endogenous Grb2 , whereas insulin had no effect
Tobe et al., J Biol Chem 1993 : Insulin stimulates association of insulin receptor substrate-1 with the protein abundant Src homology/growth factor receptor bound protein 2
Skolnik et al., EMBO J 1993 : In this report we show that in response to insulin , GRB2 forms a stable complex with two tyrosine phosphorylated proteins
Zhang-Sun et al., Endocrinology 1996 (Liver Neoplasms, Experimental) : A 60-kilodalton protein in rat hepatoma cells overexpressing insulin receptor was tyrosine phosphorylated and associated with Syp, phophatidylinositol 3-kinase, and Grb2 in an insulin dependent manner ... Studies in rat liver, muscle, and adipose tissue identified insulin dependent association of Syp, Grb2 , and p85 with tyrosine phosphorylated p60 in adipose tissue only
Ishihara et al., J Biol Chem 1997 : Insulin induced Shc phosphorylation and subsequent association with Grb2 was enhanced in WT-Shc cells
Srinivas et al., Cell Signal 1996 : alpha 2-HSG inhibits insulin induced tyrosine phosphorylation of IRS-1 and the subsequent association of GRB2 , as well as Sos, with IRS-1
Valverde et al., Mol Endocrinol 1998 : Furthermore, insulin/IGF-I stimulated IRS-1 associated Grb-2 phosphorylation
Karoor et al., J Biol Chem 1998 : The Tyr-350 -- > Phe mutant form of the beta2-adrenergic receptor, lacking the site for tyrosine phosphorylation, fails to bind Grb2 in response to insulin , fails to display internalization of beta2-adrenergic receptor in response to insulin, and is no longer subject to the counter-regulatory effects of insulin on cyclic AMP accumulation