◀ Back to AKT3

AKT3 — OPN1LW

Text-mined interactions from Literome

Sanchez et al., J Biol Chem 2007 : In contrast, we found that CBP intrinsic activity was increased by Akt through threonine 1872, a consensus site for Akt in the cysteine- and histidine-rich 3 domain of CBP, indicating that such enhanced transcriptional potential of CBP did not serve to activate ERbeta
Zeng et al., Mol Cancer Ther 2006 (Leukemia, Lymphocytic, Chronic, B-Cell...) : Furthermore, RCP168 blocked the binding of anti-CXCR4 monoclonal antibody 12G5 to surface CXCR4 in a concentration dependent manner and inhibited SDF-1alpha induced AKT and extracellular signal regulated kinase phosphorylation
Drendall et al., Protein Expr Purif 2010 : However, there is no direct evidence of Akt mediated phosphorylation of CBP
Mavila et al., PloS one 2012 (Liver Neoplasms) : FGFR activation induced cell proliferation and survival were also inhibited by the compound ICG-001, a small molecule inhibitor of ß-catenin-CREB Binding Protein (CBP) in hepatoblasts, further indicating a CBP dependent regulatory mechanism of ß-catenin activity.Conclusion : FGF signaling regulates the proliferation and survival of embryonic and transformed progenitor cells in part through AKT mediated activation of ß-catenin and downstream interaction with the transcriptional co-activator CBP