Gene interactions and pathways from curated databases and text-mining

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INS — SHC1

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

de L A Fernandes et al., Brain Res 1999 : Insulin induces tyrosine phosphorylation of the insulin receptor and SHC , and SHC/GRB2 association in cerebellum but not in forebrain cortex of rats
Xu et al., J Biol Chem 1999 : Insulin stimulation promoted the association of mIRS3 with p85, SHP2, Nck, and Shc
Ishihara et al., Biochem Biophys Res Commun 1999 : These results indicate that SHIP2 plays a negative regulatory role in insulin induced mitogenesis, and regulation of the Shc
Wada et al., Endocrinology 1999 : Although SHIP can bind via its 917/1020-Tyr residues and SH2 domain to Shc PTB domain and 317-Tyr residue, respectively, insulin induced SHIP association with Shc was more greatly decreased in 2F-SHIP cells than that in deltaSH2-SHIP cells ... 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
Páez-Espinosa et al., Mol Cell Endocrinol 1999 (Hyperinsulinism...) : Insulin induced tyrosine phosphorylation of Shc in liver, muscle and adipose tissue of insulin resistant rats ... Insulin stimulates rapid tyrosine phosphorylation of the protein Shc , which subsequently binds to Grb2, resulting in the activation of a complex mitogenic signaling network ... In fasted hypoinsulinemic rats, there was a decrease in insulin induced Shc phosphorylation in liver and adipose tissue ... The Shc-Grb2 association is directly related to the insulin induced tyrosyl phosphorylation of Shc
Sawa et al., Cell Signal 1999 (MAP Kinase Signaling System) : As previously reported, insulin induced Shc phosphorylation, Shc-Grb2 association, MAP kinase activation, and BrdU incorporation
Goldfine et al., Metabolism 2000 (Diabetes Mellitus, Type 2) : In muscle obtained during clamp studies prior to vanadium therapy, insulin stimulated the tyrosine phosphorylation of the insulin receptor, insulin receptor substrate-1 (IRS-1), and Shc proteins by 2- to 3-fold, while phosphatidylinositol 3-kinase ( PI 3-kinase ) activity associated with IRS-1 increased 4.7-fold during insulin stimulation ( P = .02 ) ... Following vanadium, there was a consistent trend for increased basal levels of insulin receptor, Shc , and IRS-1 protein tyrosine phosphorylation and IRS-1 associated PI 3-kinase, but no further increase with insulin
Nakajima et al., J Biol Chem 2000 (Carcinoma, Hepatocellular) : In contrast, insulin induced association of Shc and Grb2 was not inhibited
Goetze et al., J Biol Chem 2000 : In rat aortic VSMC, insulin induced rapid phosphorylation of the IR and Shc and caused a 5.3-fold increase in activated, phosphorylated ERK1/2 at 10 min. Insulin induced a biphasic ERK1/2 activation with a transient peak at 10 min and a sustained late phase after 2 h. Preincubation ( 30-120 min ) with TNFalpha had no effect on insulin induced IR phosphorylation ... Insulin induced phosphorylation of Shc was inhibited by TNFalpha in a similar pattern
Dominici et al., J Endocrinol 2000 : ects is associated with : ( 1 ) increased IR abundance, ( 2 ) increased insulin stimulated IR tyrosine phosphorylation, ( 3 ) normal efficiency of IRS-1 and Shc tyrosine phosphorylation and ( 4 ) normal activation of PI 3-kinase by insulin
Valverde et al., Mol Cell Biol 2001 : 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
Rocha et al., Curr Eye Res 2000 (Diabetes Mellitus, Experimental) : The activation of insulin receptors following insulin treatment, and the involvement of insulin receptor substrates-1 and -2, Shc , JAK-2 and STAT-1, were analyzed by immunoprecipitation, followed by SDS-PAGE and immunoblotting of rat lacrimal and salivary glands after exposure to insulin ... Functional studies demonstrated that insulin induced a dose dependent phosphorylation of the insulin receptor, IGF-1R, insulin receptor substrates-1 and -2, Shc , and STAT-1
Goalstone et al., J Biol Chem 2001 : Shc mediated insulin signaling to MAPK may be necessary ( but not sufficient ) for activation of prenyltransferase activity
Ishibashi et al., J Clin Invest 2001 : Insulin stimulated tyrosine phosphorylation of SHC was also reduced in ET-1 treated cells, resulting in inhibition of the MAPK pathway
Páez-Espinosa et al., Endocrine 2001 (Diabetes Mellitus, Experimental) : In the present study, we investigated the adrenergic control of insulin induced Shc phosphorylation and Shc-Grb2 association, and the modulating effect of streptozotocin induced diabetes mellitus on Shc phosphorylation and Shc/Grb2 association ... Acute treatment with epinephrine, which leads to a normoglycemic insulin-resistant state, does not affect insulin induced Shc tyrosine phosphorylation or Shc-Grb2 association in liver, muscle, or fat ... By contrast, a significant increase in insulin induced Shc phosphorylation is observed in liver and muscle of rats treated with streptozotocin ... These data suggest that while epinephrine preserves the insulin induced phosphorylation of Shc and the mitogenic pathway stimulated by Shc-Grb2 association, treatment with streptozotocin leads to a tissue-specific increase in the activity of the initial step that ultimately results in the activation of the Shc/Grb2 mitogenic pathway
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
Ugi et al., J Biol Chem 2002 : Phosphatidylinositol 3-kinase is required for insulin stimulated tyrosine phosphorylation of Shc in 3T3-L1 adipocytes ... In the current studies, we find that epidermal growth factor (EGF) and platelet derived growth factor ( PDGF ) lead to rapid phosphorylation of Shc ( maximum at 1-2 min ), whereas insulin mediated Shc phosphorylation is relatively delayed ( maximum at 5-10 min ), suggesting that an intermediary step may be necessary for insulin stimulation of Shc phosphorylation ... Because the Shc PTB domain can interact with phospholipids, we postulated that PI 3-kinase might be a necessary intermediary step facilitating insulin stimulated phosphorylation of Shc ... All three growth factors cause localization of Shc to the plasma membrane, but only the effect of insulin was inhibited by wortmannin, supporting the view that PI 3-kinase generated phospholipids mediate insulin stimulated Shc phosphorylation ... In summary, 1 ) PI 3-kinase is a necessary early step in insulin stimulated Shc phosphorylation, whereas the effects of EGF and PDGF on Shc phosphorylation are independent of PI 3-kinase
Fernandes et al., Endocrine 2001 : However, insulin induced tyrosine phosphorylation of the insulin receptor and SHC , and the association of SHC/growth factor receptor binding protein-2 ( GRB2 ) decreased significantly from d 1 to wk 60 of life in both types of tissues
Hamer et al., Diabetologia 2002 (Acanthosis Nigricans...) : Our investigation showed an impairment in insulin binding to IR ( R252C ) related mostly to a reduced affinity of the receptor for insulin and to a reduced rate of IR ( R252C ) maturation ; an inhibition of IR ( R252C ) -mediated endocytosis resulting in a decreased insulin degradation and insulin induced receptor down-regulation ; a maintenance of IR ( R252C ) on microvilli even in the presence of insulin ; a similar autophosphorylation of mutant IR ( R252C ) followed by IRS 1/IRS 2 phosphorylation, p85 association with IRS 1 and IRS 2 and Akt phosphorylation similar to those observed in cells expressing wild type IR ( IRwt ) ; and finally, a reduced insulin induced Shc phosphorylation accompanied by decreased ERK1/2 phosphorylation and activity and of thymidine incorporation into DNA in cells expressing IR ( R252C ) as compared to cells expressing IRwt
He et al., J Biol Chem 2003 (MAP Kinase Signaling System) : We report here that human melanoma M2 cells lacking FLNa expression exhibited normal insulin receptor (IR) signaling, whereas FLNa expressing A7 cells were unable to elicit insulin dependent Shc tyrosine phosphorylation and p42/44 MAPK activation despite no significant defect in IR-stimulated phosphorylation of insulin receptor substrate-1 or activation of the phosphatidylinositol 3-kinase/AKT cascade ... Insulin dependent translocation of Shc , SOS1, and MAPK to lipid raft microdomains was markedly attenuated by FLNa expression
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
Miele et al., J Biol Chem 2003 : HGA did not affect either insulin receptor kinase activity or insulin induced Shc phosphorylation on tyrosine
Mori et al., Mol Cell Endocrinol 2005 : In spite of these differences, both FL-Grb10 and the BPS-SH2 fragment inhibited insulin stimulated phosphorylation of IRS1, IRS2, Akt/PKB, Shc , ERK1/2, APS, and c-Cbl to a similar extent
Thirone et al., Diabetes 2006 (Insulin Resistance) : Insulin dependent phosphorylation of IRS1/2 and Shc was not affected by siJAK2, but insulin induced phosphorylation of the mitogen activated protein kinases ( MAPKs ) extracellular signal related kinase, p38, and Jun NH2-terminal kinase and their respective upstream kinases MKK1/2, MKK3/6, and MKK4/7 was significantly lowered when JAK2 was depleted, correlating with a significant drop in insulin mediated cell proliferation
Artemenko et al., J Cell Physiol 2007 : PDGF, but not insulin , stimulates SHIP2 tyrosine phosphorylation and its association with Shc in human and 3T3-L1 preadipocytes
Saqib et al., Journal of chemical biology 2011 : The insulin induced SHIP2 interaction with Shc is very important for the membrane localization and functioning of SHIP2
Yonezawa et al., J Biol Chem 1994 : A CHO cell line overexpressing the mutant insulin receptor, substituting Ala960 for Tyr960 and which was known to exhibit impaired tyrosine phosphorylation of IRS-1 and biological effects evoked by insulin, showed severely impaired insulin dependent tyrosine phosphorylation of Shc and moderately impaired activation of Ras ... Furthermore, insulin did not induce the association of tyrosine phosphorylated IRS-1 and Shc in CHO-IR cells
Kovacina et al., Biochem Biophys Res Commun 1993 : Insulin stimulated tyrosine phosphorylation of SHC , a SH2 containing protein, was demonstrated in Chinese hamster ovary cells overexpressing the insulin receptor by immunoblotting with antiphosphotyrosine antibodies and in vivo labeling ... Insulin induced tyrosine phosphorylation of SHC occurred very rapidly ( within 1 min ) with a dose curve which paralleled the autophosphorylation of the insulin receptor
Yamauchi et al., J Biol Chem 1994 : Expression of the insulin receptor substrate-1 (IRS1) or Shc cDNA resulted in both increased protein and insulin stimulated tyrosine phosphorylation of IRS1 and Shc proteins, respectively
Giorgetti et al., Eur J Biochem 1994 : Here we approached the insulin induced and the insulin-like-growth-factor-I induced ( IGF-I induced ) phosphorylation of SHC proteins, and the possible role of these proteins in insulin and IGF-I signaling
Pronk et al., Mol Cell Biol 1994 : Involvement of Shc in insulin- and epidermal growth factor induced activation of p21ras ... We have studied the role of Shc in insulin- and EGF induced activation of p21ras in NIH 3T3 cells overexpressing human insulin receptors ( A14 cells ) ... 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
Sasaoka et al., J Biol Chem 1994 : Thus, although both IRS-1 and Shc associate with Grb2, the current results indicate that Shc plays a more important role than IRS-1 in insulin stimulation of GNRF activity and subsequent p21ras-GTP formation
Myers et al., Mol Cell Biol 1994 : Coexpression of IRS-1 or IRS-1F-895 with the insulin receptor was required for insulin stimulated mitogenesis in 32-D cells, while expression of the insulin receptor alone was sufficient to mediate insulin stimulated tyrosine phosphorylation of Shc and activation of p21ras and mitogen activated protein ( MAP ) kinase
Pronk et al., J Biol Chem 1993 : Insulin induced phosphorylation of the 46- and 52-kDa Shc proteins
Kulas et al., J Biol Chem 1996 (Carcinoma, Hepatocellular) : Consistent with a receptor level effect, in vivo insulin dependent tyrosine phosphorylation of both IRS-1 and Shc was increased by a similar 3-fold with LAR suppression
Kulas et al., J Biol Chem 1996 : Insulin dependent tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) and Shc was 3-fold greater in CD45- cells
Li et al., Biochem Biophys Res Commun 1996 (Liver Neoplasms, Experimental) : Differential regulation of insulin stimulated tyrosine phosphorylation of IRS-1 and SHC by Wortmannin in intact cells
Ricketts et al., J Biol Chem 1996 : Functional roles of the Shc phosphotyrosine binding and Src homology 2 domains in insulin and epidermal growth factor signaling
Sasaoka et al., Endocrinology 1996 : Insulin and IGF-1 stimulated tyrosine phosphorylation of IRS-1 and Shc in a similar dose- and time dependent manner
Giorgetti-Peraldi et al., Mol Cell Biol 1997 : Insulin stimulated phosphorylation of Shc was inhibited, with no effect on IRS-1, and downstream effects on mitogen activated protein kinase and DNA synthesis were both inhibited
Ishihara et al., J Biol Chem 1997 : Insulin induced Shc phosphorylation and subsequent association with Grb2 was enhanced in WT-Shc cells ... Likewise, reduction of endogenous Shc expression by antisense Shc mRNA resulted in increased insulin stimulation of IRS-1 phosphorylation
Srinivas et al., Cell Signal 1996 : In a parallel pathway, alpha 2-HSG also inhibits insulin induced tyrosine phosphorylation of Shc
Kao et al., Endocrinology 1997 : Insulin stimulates the phosphorylation of the 66- and 52-kilodalton Shc isoforms by distinct pathways ... Alkaline phosphatase treatment and direct phosphoamino acid analysis demonstrated that insulin stimulated an increase in serine phosphorylation of the 66-kDa isoform but not 52-kDa Shc , although the latter displayed a marked increase in tyrosine phosphorylation
Sharma et al., Mol Cell Biol 1997 : In both cell types, overexpression of either the PTB or the SAIN protein caused a significant decrease in insulin induced tyrosine phosphorylation of IRS-1 and Shc proteins, IRS-1 associated phosphatidylinositol 3-kinase (PI 3-K) enzymatic activity, p70s6k activation, and p44 and p42 mitogen activated protein kinase ( MAPK ) phosphorylation ... Thus, interference with the IRS-1-IR interaction inhibits insulin stimulated IRS-1 and Shc phosphorylation, PI 3-K enzymatic activity, p70s6k activation, MAPK phosphorylation and cell cycle progression
Thirone et al., FEBS Lett 1998 : Regulation of insulin stimulated tyrosine phosphorylation of Shc and IRS-1 in the muscle of rats : effect of growth hormone and epinephrine ... In contrast, no change is observed in insulin stimulated Shc tyrosine phosphorylation, or in the association of this substrate with Grb2
Jacob et al., J Biol Chem 1998 : The negative effect of RPTPalpha on insulin activation of the prolactin promoter is not due to reduced phosphorylation or kinase activity of the insulin receptor or to reduced phosphorylation of insulin receptor substrate-1 or Shc
Ceresa et al., Mol Cell Biol 1998 : In contrast, expression of K44A/dynamin partially inhibited insulin stimulated Shc tyrosine phosphorylation and activation of the mitogen activated protein kinases ERK1 and -2
Páez-Espinosa et al., Endocrine 1998 : Insulin induces tyrosine phosphorylation of Shc and stimulates Shc/GRB2 association in insulin-sensitive tissues of the intact rat ... In this study, we used immunoprecipitation and immunoblotting to examine the effect of insulin on Shc tyrosine phosphorylation and Shc/GRB2 association in insulin-sensitive tissues of the intact rat
Tsakiridis et al., J Biol Chem 1998 : We conclude that the actin filament network plays an essential role in insulin regulation of Shc dependent signaling events governing gene expression by facilitating the interaction of Shc with Grb2
Páez-Espinosa et al., Braz J Med Biol Res 1998 : Insulin induces tyrosine phosphorylation of Shc in cell cultures and in insulin-sensitive tissues of the intact rat