Gene interactions and pathways from curated databases and text-mining

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AKT3 — SMAD3

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
Song et al., EMBO J 2006 : Novel roles of Akt and mTOR in suppressing TGF-beta/ALK5 mediated Smad3 activation
Horowitz et al., Cell Signal 2007 : Here, we demonstrate that FAK and AKT are independently regulated by early activation of SMAD3 and p38 MAPK, respectively
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
Dumaresq-Doiron et al., J Cell Physiol 2012 : At the molecular level, immature Hyal-1 null mice have decreased mRNA expression of follistatin and higher levels of phospho-Smad3 protein, resulting in increased levels of phospho-Akt in pubertal mice
Suwanabol et al., Am J Physiol Heart Circ Physiol 2012 (Carotid Artery Injuries) : Overexpression of Smad3 enhanced p38 phosphorylation and inhibition of p38 with a chemical inhibitor or a small interfering RNA blocked TGF-ß induced Akt phosphorylation ... Our findings were confirmed in vivo where overexpression of Smad3 in a rat carotid injury model led to enhancement of p-p38, p-Akt , as well as SMC proliferation
Winbanks et al., J Cell Biol 2012 (Hypertrophy) : Expression of constitutively active Smad3 not only markedly prevented skeletal muscle growth induced by follistatin but also potently suppressed follistatin induced Akt/mTOR/S6K signaling
Han et al., Int J Biochem Cell Biol 2013 : In addition, Smad activation inhibits muscle protein synthesis by suppressing Akt signaling