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EIF4EBP1 — IGF1

Text-mined interactions from Literome

Shen et al., J Endocrinol 2005 : Both LY294002 and rapamycin blocked the insulin and IGF-I induced increases in 4EBP1 phosphorylation
Vary et al., Am J Physiol Regul Integr Comp Physiol 2006 (Sepsis) : IGF-I increased the phosphorylation of translation repressor 4E-binding protein-1 (4E-BP1)
Shen et al., Pediatr Res 2005 : The IGF-I induced increase in 4E-BP1 phosphorylation ( percentage in the gamma form ) increased from 28 % in control to 44 % ( NS )
Shigeyama et al., Mol Cell Biol 2008 (Hyperinsulinism) : Here, we show that mice deficient in TSC2, specifically in pancreatic beta cells ( betaTSC2 ( -/- ) mice ), manifest increased IGF-1 dependent phosphorylation of p70 S6 kinase and 4E-BP1 in islets as well as an initial increased islet mass attributable in large part to increases in the sizes of individual beta cells
Cao et al., Science signaling 2009 : Loss of Galpha ( i1 ) and Galpha ( i3 ) severely impaired the activation of Akt and of p70 S6 kinase and 4E-BP1 , downstream targets of mTORC1, in response to EGF, heparin binding EGF-like growth factor, and transforming growth factor alpha, but not insulin, insulin-like growth factor , or platelet derived growth factor
Jacobson et al., Br J Cancer 2009 (Mesothelioma) : An inhibitor of Akt diminished IGF-I mediated phosphorylation of 4E-BP1 , whereas inhibiting MAPK signalling had no such effect
Graves et al., Proc Natl Acad Sci U S A 1995 : The effects of PDGF and IGF-I on increasing PHAS-I phosphorylation, on dissociating the PHAS-I-eIF-4E complex, and on increasing p70S6K were abolished by rapamycin
Xu et al., J Biol Chem 1998 : In addition, we find that amino acids are necessary for insulin-like growth factor ( IGF-I ) to stimulate the phosphorylation of PHAS-I indicating that a requirement for amino acids may be essential for other beta-cell growth factors in addition to insulin and IGF-I to activate this signaling pathway