Gene interactions and pathways from curated databases and text-mining

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IGF2 — PI3

Text-mined interactions from Literome

Lawlor et al., Mol Cell Biol 2000 (MAP Kinase Signaling System) : Transient transfection of a constitutively active PI3-kinase or an inducible Akt promoted myoblast viability in the absence of growth factors, while inhibition of PI3-kinase activity by the drug LY294002 selectively blocked IGF- but not PDGF mediated muscle cell survival
Cheng et al., J Biol Chem 2000 (MAP Kinase Signaling System) : In parallel, IGF-I activates IGF-I receptor, insulin receptor substrate-1 (IRS-1), phosphatidylinositol 3 (PI-3)-kinase , and FAK
Pozios et al., Am J Physiol Regul Integr Comp Physiol 2001 (MAP Kinase Signaling System) : These results indicate that both IGF-I and -II are potent mitogens for zebrafish embryonic cells and that activation of both the MAPK and PI3 kinase signaling pathways is required for the mitogenic action of IGFs in zebrafish embryonic cells
Strle et al., J Neuroimmunol 2002 : In contrast to IL-10, IGF-I increases enzymatic activity of PI 3-kinase and causes phosphorylation on serine ( 473 ) of Akt but does not prevent microglial apoptosis
Galvan et al., J Biol Chem 2003 : IGF-IR binding to its ligand, insulin-like growth factor ( IGF-I ) activates phosphoinositide 3-kinase (PI3K) , promotes cell proliferation by activating the mitogen activated protein kinase ( MAPK ) cascade, and blocks apoptosis by inducing the phosphorylation and inhibition of proapoptotic proteins such as BAD
Lassarre et al., Endocrinology 2003 (Breast Neoplasms) : However, IGF-I induced PI 3-kinase activity was decreased by 24 h of pretreatment with EGF or PDGF but not with FGF
Kataoka et al., J Radiat Res 2004 : We have investigated the role of insulin-like growth factor I receptor ( IGF-IR ) in heat shock induced activation of the mitogen activated protein kinase ( MAPK ) and phosphatidylinositol-3 ' kinase (PI3-K) pathways
Itakura et al., J Neurochem 2005 : In striking contrast, IGF-1 activated the PI3-kinase pathway but not the MAPK pathway, and IGF-1 dependent enhancement was suppressed by a PI3-kinase inhibitor but not by a MAPK kinase inhibitor
Lackey et al., Oncogene 2007 : These effects on IGF/insulin signaling include a reduction of up to five- to tenfold in IGF stimulated PI 3-kinase activation, a failure to activate the ERK kinases and, in some cells, reduced expression of insulin receptor substrate 1, and both IGF1 and insulin receptors
Fukushima et al., Endocrinology 2008 : In contrast, IGF-I dependent PI 3-kinase activation was required for the increase in cyclin D1 mRNA levels and degradation of p27 ( Kip1 )
Pinzon-Guzman et al., J Neurosci 2011 : In adult retinas, IGF1 activates PI-3 kinase (PI3K) , but in neonatal retinas its action is identical to the action of an PI3K inhibitor
King et al., Journal of ovarian research 2013 : This may be due partly to altered collagen IV deposition and organization in the ovary in response to insulin and IGF signaling mediated by PI 3-kinase
Pomerance et al., J Neurosci Res 1995 : In astroglial cells cultured in serum-free medium, IGF1 , PDGF, and EGF, which stimulate cell proliferation, increased PI(3)-kinase activity immunoprecipitated with anti-phosphotyrosine antibodies as shown by thin layer chromatography and high performance liquid chromatography
Kornmann et al., Cancer Res 1998 (Colonic Neoplasms...) : Insulin, IGF-I , and IGF-II enhanced the growth of both cell lines, stimulated tyrosine phosphorylation of IRS-2, and increased IRS-2 associated phosphatidylinositol (PI) 3-kinase activity ... Insulin, IGF-I, and IGF-II enhanced the growth of both cell lines, stimulated tyrosine phosphorylation of IRS-2, and increased IRS-2 associated phosphatidylinositol (PI) 3-kinase activity
Hayashi et al., J Biol Chem 1998 : In cultured cells, IGF-I specifically activated phosphatidylinositol 3-kinase ( PI3-kinase ) and its downstream target, protein kinase B, but not mitogen activated protein kinases