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AKT2 — CDH13

Text-mined interactions from Literome

Joshi et al., FASEB J 2007 : ILK-siRNA abolished T-cad dependent effects on ( Ser-473 ) Akt/ ( Ser-9 ) GSK3beta phosphorylation, active beta-catenin accumulation, and survival
Zhou et al., Mol Cancer Ther 2009 (Lung Neoplasms...) : Luteolin inhibits mdm2 through AKT and overexpression of active AKT attenuated luteolin induced expression of E-cadherin , suggesting that luteolin regulates E-cadherin through AKT/mdm2 pathway
Joshi et al., FASEB J 2009 : Similarly to overexpression of native T-cad, cells expressing DeltaII, DeltaIII, or DeltaIV displayed elevated levels of p-Akt and p-GSK3beta and increased proliferation rates ( for DeltaII, DeltaIII ) vs. E. DeltaI- and DeltaV transduced cells exhibited reduced levels of p-Akt and p-GSK3beta and retarded growth rates vs. E. Stimulatory effects of native T-cad overexpression on Akt and GSK3beta phosphorylation were dose dependently inhibited by coexpression of DeltaI or DeltaV
Philippova et al., Eur Heart J 2011 (Coronary Artery Disease) : Gain-of-function and loss-of-function studies demonstrate that MP-bound T-cad induced Akt phosphorylation and activated angiogenic behaviour in target ECs via homophilic based interactions
Cheng et al., J Clin Endocrinol Metab 2012 : Moreover, the inhibition of EGF induced ERK1/2, p38, and Akt activation by pharmacological inhibitors attenuated EGF induced Slug expression and the down-regulation of E-cadherin , as well as subsequent cell invasion
Kisslov et al., Biochim Biophys Acta 2012 (Colonic Neoplasms) : AS or Ly294002, but not H-89, decreased PKB/Akt activation as well as the nuclear localization of ß-catenin and cyclin D1 and increased the plasma membrane localization of ß-catenin with E-cadherin , suggesting that these processes are regulated by the PKB pathway