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IGF1 — SMAD3

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: SMAD3 → IGF1 (decreases, IGF1 Activity) Song et al., J Biol Chem 2003*
  Evidence: The phosphatidylinositol 3-kinase (PI3K) inhibitor, LY29004 reverses the ability of IGF-I to inhibit TGF-beta-induced transcriptional responses and the activation of Smad3, suggesting that the suppression of TGF-beta signaling by IGF-I is mediated through activation of PI3K. Moreover, we show that enforced expression of dominant-negative PI3K (DN-p85alpha) or phosphatidylinositol 3-phosphate-phosphatase, PTEN, also reverse the suppressive effect of IGF-I on TGF-beta-induced 3TP-luciferase report...

Text-mined interactions from Literome

Fanayan et al., J Biol Chem 2002 (Breast Neoplasms) : We previously demonstrated in T47D cells transfected to express the transforming growth factor-beta receptor type II ( TGF-betaRII ) that insulin-like growth factor binding protein-3 ( IGFBP-3 ) could stimulate Smad2 and Smad3 phosphorylation, potentiate TGF-beta1 stimulated Smad phosphorylation, and cooperate with exogenous TGF-beta1 in cell growth inhibition ( Fanayan, S., Firth, S. M., Butt, A. J., and Baxter, R. C. ( 2000 ) J. Biol. Chem. 275, 39146-39151 )
Song et al., J Biol Chem 2003 : However, Western blot analysis reveals that IGF-I selectively inhibits the TGF-beta triggered activation Smad3 but not Smad2, while not altering expression of total Smads 2, 3, or 4
Elliot et al., J Am Soc Nephrol 2006 (Albuminuria...) : In addition, Smad3 activation was stimulated by IGF-I and blocked by LY294002, suggesting cross-talk between Smad and the phosphatidylinositol-3 kinase/AKT pathways
Dong et al., Am J Physiol Endocrinol Metab 2013 (Fibrosis) : Using immunoprecipitation assay, we found an interaction between p-Akt or Akt with Smad3 in wild-type mouse muscles and in C2C12 myoblasts ; importantly, IGF-I increased p-Akt and Smad3 interaction, whereas TGF-ß1 decreased it