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GSK3B — SMAD3
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Guo et al., Genes Dev 2008
:
Reduction in the expression or activity of
Axin/GSK3-beta leads to increased
Smad3 stability and transcriptional activity without affecting TGF-beta receptors or Smad2, whereas overexpression of these proteins promotes Smad3 basal degradation and desensitizes cells to TGF-beta ... Mechanistically, Axin facilitates
GSK3-beta mediated phosphorylation of
Smad3 at Thr66, which triggers Smad3 ubiquitination and degradation
Hua et al., Eur J Pharmacol 2010
:
These results uncovered a novel mechanism for the
GSK3beta negative
regulation of
TGF-beta1/Smad3 and Angiotensin II/Smad3 mediated transcription and apoptosis by the identification of a crosstalk between GSK3beta and Smad3 signal pathway