Gene interactions and pathways from curated databases and text-mining

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IGF1 — WNK1

Text-mined interactions from Literome

Vitari et al., Biochem J 2004 (Hypertension...) : Consistent with PKB mediating this phosphorylation, inhibitors of PI 3-kinase ( phosphoinositide 3-kinase ; wortmannin and LY294002 ) but not inhibitors of mammalian target of rapamycin ( rapamycin ) or MEK1 ( mitogen activated protein kinase kinase-1 ) activation ( PD184352 ), inhibited IGF1 induced phosphorylation of endogenous WNK1 at Thr-60 ... Moreover, IGF1 induced phosphorylation of endogenous WNK1 did not occur in PDK1-/- ES ( embryonic stem ) cells, in which PKB is not activated ... In contrast, IGF1 still induced normal phosphorylation of WNK1 in PDK1 ( L155E/L155E ) knock-in ES cells in which PKB, but not S6K ( p70 ribosomal S6 kinase ) or SGK1 ( serum- and glucocorticoid induced protein kinase 1 ), is activated
Xu et al., J Biol Chem 2005 (Hypertension) : Finally, we show that WNK1 is required for the activation of SGK1 by insulin-like growth factor 1
Wu et al., J Biol Chem 2008 : In rat growth plate chondrocytes, IGF-I induced NF-kappaB-p65 nuclear translocation ... In rat growth plate chondrocytes, IGF-I induced NF-kappaB-p65 nuclear translocation
Yang et al., Biochem J 2011 (Colonic Neoplasms) : IGF-1 increased the expression of c-Jun, FosB, MafG, p65 , c-Myb, E2F-1 and YY1 at the pre-translational level
Wu et al., J Biol Chem 2011 : Lastly, the inhibition of Stat5b expression in chondrocytes prevented the GH promoting effects on NF-?B-DNA binding, whereas the inhibition of NF-?B p65 expression or activity prevented the GH-dependent activation of IGF-1 and bone morphogenetic protein-2 expression