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AKT3 — SMAD2

Text-mined interactions from Literome

Song et al., J Biol Chem 2003 : Insulin-like growth factor-I inhibits transcriptional responses of transforming growth factor-beta by phosphatidylinositol 3-kinase/Akt dependent suppression of the activation of Smad3 but not Smad2
Lee et al., Biochem Biophys Res Commun 2004 : In addition, PI3K inhibitor, dominant negative Akt , and dominant negative ILK could not block TGFbeta mediated C-terminal phosphorylation of Smad2
Sun et al., Cytokine 2006 : Furthermore, both the PI3K inhibitor LY294002 and the dominant negative AKT ( DN-AKT ) abolished the inhibitory effects of insulin, demonstrating that the inhibition of Smad2 activation by insulin was PI3K/AKT dependent
Xia et al., American journal of physiology. Renal physiology 2008 (Hyperglycemia) : In high glucose, Akt Ser473 phosphorylation appeared within 1 h and Smad2/3 nuclear translocation was prevented with neutralizing TGF-beta(1) antibodies
Graham et al., Prostate 2009 (Neoplasm Metastasis...) : PI3K/Akt dependent transcriptional regulation and activation of BMP-2-Smad signaling by NF-kappaB in metastatic prostate cancer cells
Sweetwyne et al., Am J Pathol 2010 : Collagen stimulation was independent of TGF-ß activity and Smad phosphorylation but was blocked by an Akt inhibitor, suggesting that signaling through the Akt pathway is important for regulation of collagen through TSP1 binding to calreticulin
Osman et al., Growth Factors 2011 : TGF-ß induced a rapid phosphorylation of Akt that continued upto 4 h. Akt phosphorylation was blocked by Akt1/2 inhibitor SN30978 ; however, it did not block Smad2 phosphorylation at either the carboxy or linker regions indicating that TGF-ß mediated Akt phosphorylation is independent of Smad2 signalling
Han et al., Int J Biochem Cell Biol 2013 : In addition, Smad activation inhibits muscle protein synthesis by suppressing Akt signaling