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CDK4 — 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
Zhang et al., J Neurosurg 2006
(Glioma) :
Overall, the expression of the Smad2 and
Smad3 proteins was low in the glioma cell lines, the phosphorylation and nuclear translocation of Smad2 and Smad3 were impaired, and the TGFbeta receptor signal did not
affect the expression of the SnoN, p21, p15, cyclin D1, and
CDK4 proteins
Zelivianski et al., Mol Cancer Res 2010
(Breast Neoplasms) :
Cyclin dependent kinase 4-mediated phosphorylation
inhibits Smad3 activity in cyclin D-overexpressing breast cancer cells ... We hypothesized that overexpression of cyclin D1 exerts tumorigenic effects in breast cancer cells through
CDK4 mediated phosphorylation and
inhibition of
Smad3 and release of G ( 1 ) arrest ... Smad3 transcriptional activity and cell cycle control were examined in cells transfected with wild-type ( WT )
Smad3 or Smad3 with single or multiple CDK phosphorylation site mutations ( M ) in the
presence or absence of the
CDK4 inhibitor or cotransfection with cdk4 small interfering RNA ( siRNA )
Cheng et al., Chem Biol 2012
(MAP Kinase Signaling System) :
We found that indirubin derivative E738 inhibited both TGFß and BMP pathways through ubiquitin-proteasome mediated depletion of total R-Smad pools, although
phospho-R-Smad levels were initially
stabilized by GSK3ß and
cyclin dependent kinase inhibition