IndraLab
Statements
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."
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."
sparser
"Another study from the same group [ xref ] established that phosphorylation of AKT on Thr308 and Ser473 increases following treatment of ALL cells with AICAR and demonstrated that AKT phosphorylation on Thr 308 is mediated by AMPK-induced IGF-1R activation and phosphorylation of IRS-1."
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."
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"In support of this hypothesis, we report here that : (1) IRS-1 expression increases cell adhesion and decreases cell motility; (2) over-expression of the IGF-IR, in the absence of IRS-1, causes growth arrest and (3) a combination of IGF-IR and IRS-1 restores the transformed phenotype of LNCaP cells."
reach
"To investigate the roles of TGFbeta and IGF signaling pathways in miR-130a and miR-145 regulations of myeloid immune function, overexpression constructs of Tgfbr2, Igf1r, and Irs1 without 3 '-UTR were utilized to prevent the mRNA degradation of TbetaRII, IGF1R and IRS1 in Gr-1 + CD11b + cells by miR-130a or miR-145."
reach
"IGF-1 and IGF-1R induces differentiation rather than proliferation when the cells do not express or underexpress insulin receptor substrate-1 (IRS-1), a docking protein for both IGF-1R and the insulin receptor that is known to send a mitogenic, anti-apoptotic and anti-differentiation signal XREF_BIBR XREF_BIBR."
reach
"These results suggested that the decreases in IRS-1 and IGF signaling by IGF-I receptor downregulation could be crucial for cell differentiation.L6 myoblasts that highly expressed IRS-1 protein were eliminated from the cell layer upon culturing with normal cells due to sustained activation of the IGF-I receptor on the plasma membrane."