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AKT1 — WNT1

Text-mined interactions from Literome

Dihlmann et al., Carcinogenesis 2005 (Colonic Neoplasms...) : Accordingly, we hypothesized that AKT1 expression might be regulated by Wnt/beta-catenin signaling
Yang et al., Oncogene 2006 (Prostatic Neoplasms) : The reduction of hAR protein is consistent with evidence that Wnt signaling increased phosphorylation of Akt and its downstream target, MDM2 that promotes degradation of hAR protein through a proteasomal pathway
Raucci et al., J Cell Physiol 2008 : Wnt signals, that promotes differentiation, also induce AKT phosphorylation, and cells expressing active AKT have increased levels of stabilized beta-catenin, a central molecule in Wnt signaling
Case et al., J Biol Chem 2008 : In summary, mechanical strain activates Akt and inactivates GSK3beta to allow beta-catenin translocation, and Wnt signaling through LRP5 is not required for these strain mediated responses
Lee et al., Oncogene 2009 (Breast Neoplasms) : Id-1 activates Akt mediated Wnt signaling and p27 ( Kip1 ) phosphorylation through PTEN inhibition
Sonderegger et al., Endocrinology 2010 : Chemical inhibition of PI3K abolished Wnt dependent phosphorylation of AKT and GSK-3beta and trophoblast motility but did not affect appearance of activated beta-catenin or Wnt/TCF reporter activity
Sunters et al., J Biol Chem 2010 : Mechano-transduction in osteoblastic cells involves strain regulated estrogen receptor alpha mediated control of insulin-like growth factor (IGF) I receptor sensitivity to Ambient IGF, leading to phosphatidylinositol 3-kinase/AKT dependent Wnt/LRP5 receptor independent activation of beta-catenin signaling
Chong et al., Curr Neurovasc Res 2011 (Diabetes Mellitus, Experimental...) : EPO relies upon novel signaling of Wnt1 that requires Akt1 , FoxO3a, GSK-3ß, and ß-catenin to foster vascular integrity during experimental diabetes
Rybchyn et al., J Biol Chem 2011 : An Akt dependent increase in canonical Wnt signaling and a decrease in sclerostin protein levels are involved in strontium ranelate induced osteogenic effects in human osteoblasts
Kumar et al., Carcinogenesis 2012 (Colonic Neoplasms...) : Expression of constitutively active myristoylated-Akt or inactivation of GSK3ß using LiCl attenuated SD-mediated inhibition of Wnt transcriptional activity and active-ß-catenin levels
Gui et al., J Cell Biochem 2013 : Results showed that Wnt3a rapidly activated Wnt/ß-catenin signaling, promoted IRS2 expression and Akt phosphorylation in NIT-1 cells