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IGF1R — PI3

Text-mined interactions from Literome

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
Duarte et al., Biochim Biophys Acta 2008 : Thus, insulin mediated activation of IR/IGF-1R stimulates PI-3K/Akt and inhibits GSK-3beta signaling pathways, modifying neuronal antioxidant defense-, glucose metabolism- and anti-apoptotic associated protein synthesis
Hu et al., Cancer Res 2008 (Carcinoma...) : Investigation of IGF1R mediated signaling pathways using small interfering RNA approaches indicated that, as expected, phosphatidylinositol 3'-kinase (PI3K) was activated by IGF1R
Furundzija et al., Biochem Biophys Res Commun 2010 (Atherosclerosis) : Pharmacological blocking experiments with specific inhibitors of Akt, PKC and p38 MAP-kinase revealed that IGF-1 dependent activation of focal adhesion kinase ( FAK ) and paxillin, and consecutively IGF-1 facilitated migration, required IGF-1/IGF-1R mediated PI3-kinase/PKC/p38 dependent integrin inside-out signaling
Kato et al., J Cell Physiol 1993 : Overexpression of the IGF-I receptor did not affect sensitivity or maximal responsiveness of glucose uptake or PI3 kinase activation to IGF-I
Li et al., Exp Cell Res 1998 : A well characterized substrate of the IGF-1 R, IRS-1, is constitutively phosphorylated by the Delta870-905 IGF-1 R and phosphoinositide (PI) 3-kinase activity, which is normally activated by the phosphorylation of IRS-1 following IGF-1 stimulation, is increased even in the absence of IGF-1