Gene interactions and pathways from curated databases and text-mining

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IGF1 — RUNX2

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Pei et al., Acta Pharmacol Sin 2003 (MAP Kinase Signaling System) : IGF-I , GM-CSF, and EGF could increase the promoter activity and the mRNA expression of murine Cbfalpha1 gene in MC3T3-E1 and C2C12 cells
Qiao et al., J Biol Chem 2004 : Insulin-like growth factor-1 regulates endogenous RUNX2 activity in endothelial cells through a phosphatidylinositol 3-kinase/ERK dependent and Akt independent signaling pathway ... Here we show that IGF-1 and its receptor regulate post-translational changes in RUNX2 to activate DNA binding in proliferating EC ... The phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002, reduced both basal and IGF-1 stimulated RUNX2 DNA binding activity in the absence of changes in RUNX2 protein as did the overexpression of the phosphatidylinositol 3-phosphate phosphatase, confirming that PI3K signaling mediates RUNX2 activation ... Treatment with U0126, which inhibits ERK1/2 activation, reduced IGF-1 stimulated RUNX2 DNA binding without affecting RUNX2 protein levels ... Surprisingly, these IGF-1 mediated effects on RUNX2 were not regulated by Akt phosphorylation, a common downstream target of PI3K, as determined by pharmacological or genetic inhibition ... However, an inhibitor of the p21 activated protein kinase-1, glutathione S-transferase-Pak1- ( 83-149 ), inhibited both basal and IGF-1 stimulated RUNX2 DNA binding, suggesting that Pak1 mediates IGF-1 signaling to increase RUNX2 activity ... These results indicate that the angiogenic growth factor, IGF-1 , can regulate RUNX2 DNA binding through sequential activation of the PI3K/Pak1 and ERK1/2 signaling cascade
Ochiai et al., J Biol Chem 2012 (Bone Diseases) : Inhibition of IGF-1 signaling using small interfering RNA ( siRNA ) against insulin receptor substrate-1 (IRS-1) suppressed mRNA expression of RUNX2 , ALP, BSP, and IGF-1 even with single TGF-ß1 administration