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AKT3 — WNT1
Text-mined interactions from Literome
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
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