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AKT2 — GJA1

Text-mined interactions from Literome

Yao et al., Ophthalmic Res 2008 : The activation of PI3K/Akt was necessary for the TGF-beta(2) stimulated downregulation of connexin 43 , which in turn was necessary for TGF-beta2 induced EMT in HLEB-3 cells
Tacheau et al., J Cell Physiol 2008 : Using specific pharmacologic inhibitors for JNK, ERK, p38, and PI3K/AKT signaling pathways, we demonstrated the cooperative role of p38 and PI3K/AKT signaling in TGF-beta1 induced Cx43 expression and gap junctional communication
Bhattacharjee et al., Biochem Biophys Res Commun 2009 : Furthermore, dominant negative Akt expression reduced both Cx43 expression and gap junction activity ... These results suggest an important role of PI3K/Akt in the regulation of basal Cx43 expression
Kim et al., J Cell Physiol 2010 : We conclude that NECA stimulated Cx43 phosphorylation mediated by PI3K/Akt , PKC, MAPKs, and NF-kappaB, which subsequently stimulated cell migration and proliferation through Src, integrin beta1, FAK, and paxillin signal pathways
Liu et al., Nephrol Dial Transplant 2012 (Hyperglycemia...) : Cx43 overexpression could prevent PTEN inhibition, Akt and mTOR phosphorylation, resulting in restoration of cell cycle and proliferation ability and reversion of GMC hypertrophy ... PTEN/Akt/mTOR signaling stimulated by high concentration of glucose is regulated by Cx43 overexpression, which unveils part of the molecular mechanism of Cx43 in regulating hyperglycemia induced hypertrophy