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IndraLab

Statements

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phosphosite cbn pc11 biopax bel_lc signor biogrid tas lincs_drug hprd trrust | geneways tees isi trips rlimsp medscan sparser reach
reading

IGF1R activates IRS1. 10 / 38
10 | 4 22
reach
"Clemmons et al. have shown that, under normoglycemic conditions, stimulation of the IGF-IR expressed on vascular smooth muscle cells and vascular endothelial cells only activates IRS-1 leading to stimulation of the " metabolic " (phosphoinositide 3) PI-3 kinase pathway, but not to stimulation of the " mitogenic " (mitogen activated protein) MAP kinase pathway."
reach
"Similarly, mammalian target of rapamycin (m-TOR) inhibitors can activate PI3K-Akt pathway via loss of negative feedback on IRS-1 (insulin receptor substrate -- 1), an effect that can be suppressed by IGF-1R blockade [XREF_BIBR - XREF_BIBR]."
reach
"Under normoglycemic conditions vascular smooth muscle and endothelial cells are cystostatic and stimulation of the IGF-I receptor activates the adaptor protein IRS-1 which leads to PI-3 kinase pathway activation."
reach
"These cells lack IRS-1 and -2 expression, yet express functional IGF-IR, allowing us to investigate whether IGF-IR activation stimulates cell proliferation and motility in the absence of IRS-1 and -2."
reach
"Inhibition of IGF-IR signaling disrupted the association of IRS-1 with PI3K and restored the ability of gefitinib to down-regulate PI3K and AKT signaling and to inhibit cell growth."
signor
"Binding of IGF1 to its receptor leads to activation of its intrinsic tyrosine kinase and autophosphorylation, thus generating docking sites for insulin receptor substrate (IRS), which is also phosphorylated by the IGF1 receptor."
reach
"This study further suggested that phosphorylation of Ob-R and IGF-IR subsequently activated downstream signaling molecules Akt, ERK, IRS-1, and IRS-2."
sparser
"This review discusses recently published data regarding the ability of hyperglycemia to sensitize cells that are capable of dedifferentiating to the growth promoting effects of IGF-I. Under normoglycemic conditions vascular smooth muscle and endothelial cells are cystostatic and stimulation of the IGF-I receptor activates the adaptor protein IRS-1 which leads to PI-3 kinase pathway activation."
reach
"Tyrosine phosphorylation of IGF-1R upon extracellular ligand binding induces the activation of insulin receptor substrate 1 that can provide sufficient binding of initial effector associated tyrosine phosphorylation genes with an SH2-domain, such as PI3K, Shc and Grb2, through pleckstrin homology and phosphotyrosine binding domains XREF_BIBR, XREF_BIBR."
signor
"Furthermore, IGF-1 stimulates tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-2 and their association with the p85 subunit of phosphoinositide-3 kinase (PI3K)."
IGF1R phosphorylated on Y1166 activates IRS1. 1 / 1
1 |
bel
"We have studied the effect of double tyrosine mutations on IGF-I induced receptor autophosphorylation, activation of Shc and IRS-1 pathways, and cell proliferation and tumorigenicity. Substitution of tyrosines 1131/1135 blocks any detectable autophosphorylation, whereas substitution of tyrosines 1131/1136 or 1135/1136 only reduces autophosphorylation levels in some clones by approximately 50%. Nevertheless, all the cells expressing IGF-I receptors with double tyrosine substitutions demonstrated markedly reduced signaling through Shc and IRS-1 pathways. "