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AKT3 — RHO

Text-mined interactions from Literome

Genot et al., Mol Cell Biol 2000 : We show that in Jurkat cells, activated forms of Rac1 or Cdc42, but not Rho , stimulate an increase in Akt/PKB activity
Baudhuin et al., Mol Pharmacol 2002 : In contrast to S1P and PDGF, LPA requires Rho for Akt S473 phosphorylation, and Rho is upstream of phosphatidylinositol 3-kinase (PI3-K)
Cosentino et al., Recenti Prog Med 2003 (Acute Disease...) : Recent findings on statin induced inhibition of Rho/Rho-kinase and activation of Akt provide new insights into the protective action of statins in acute coronary syndromes
Wolfrum et al., Arterioscler Thromb Vasc Biol 2004 (Heart Diseases...) : Inhibition of Rho-kinase leads to rapid activation of phosphatidylinositol 3-kinase/protein kinase Akt and cardiovascular protection ... In human endothelial cells, the Rho-kinase inhibitor, hydroxyfasudil ( HF) (1 to 100 micromol/L ), increased Akt serine-473 phosphorylation within 15 minutes, leading to a 2.2-fold and 4.0-fold increase in Akt kinase activity and nitric oxide ( NO ) release, respectively
Stepan et al., Am J Physiol Gastrointest Liver Physiol 2004 : G17 induction of Akt activation was reduced by > 60 % by both dominant negative Ras and Rho and by 30 % by dominant negative Cdc42
Kim et al., Blood 2006 : Selective G ( 12/13 ) activation resulted in Src kinase activation, and Akt phosphorylation induced by costimulation of G ( 12/13 ) and Gi/Gz was inhibited by a Src kinase inhibitor but not by a Rho kinase inhibitor
Ueno et al., J Biol Chem 2006 (Carcinoma, Renal Cell...) : NEU3 silencing by siRNA resulted in the opposite : decreased Akt phosphorylation and inhibition of Rho activation
Sugimoto et al., Biochem Biophys Res Commun 2007 : Inhibition of Rho-kinase , an effector of the small GTPase RhoA, leads to activation of Akt/PKB , which phosphorylates eNOS at Ser1177 and thereby promotes NO production
Anegawa et al., Hepatology 2008 (Disease Models, Animal...) : These results show in secondary biliary cirrhosis that ( 1 ) Rho-kinase activation with resultant eNOS down-regulation is substantially involved in the pathogenesis of portal hypertension and ( 2 ) Rho-kinase might interact with Akt and subsequently inhibit the binding of Akt to eNOS
Du et al., Cancer Res 2010 (Carcinoma, Lewis Lung...) : Here, we report that the distinct receptor S1P(2) is responsible for mediating the G ( 12/13 ) /Rho dependent inhibitory effects of S1P on Akt , Rac, and cell migration, thereby negatively regulating tumor angiogenesis and tumor growth
Takuwa et al., Biofactors 2012 : In addition, S1P(1) mediates stimulation of cell proliferation through the G ( i ) -mediated signaling pathways including phosphatidylinositol 3-kinase (PI3K)/Akt and ERK whereas S1P(2) mediates inhibition of cell proliferation through mechanisms involving G ( 12/13 ) /Rho/Rho kinase/PTEN dependent Akt inhibition