◀ Back to SMAD3
CTNNB1 — SMAD3
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
CTNNB1
—
SMAD3
(physical association, affinity chromatography technology)
Tian et al., Am J Pathol 2002*
-
IRef Biogrid Interaction:
CTNNB1
—
SMAD3
(physical association, affinity chromatography technology)
Dahle et al., Science signaling 2010*
-
IRef Biogrid Interaction:
CTNNB1
—
SMAD3
(physical association, affinity chromatography technology)
Charbonney et al., Mol Biol Cell 2011*
-
IRef Biogrid Interaction:
CTNNB1
—
SMAD3
(physical association, affinity chromatography technology)
Zhou et al., J Biol Chem 2012*
-
IRef Hprd Interaction:
CTNNB1
—
SMAD3
(in vitro)
Tian et al., Am J Pathol 2002*
-
IRef Ophid Interaction:
SMAD3
—
CTNNB1
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
-
IRef Ophid Interaction:
SMAD3
—
CTNNB1
(aggregation, confirmational text mining)
Tian et al., Am J Pathol 2002*
Text-mined interactions from Literome
Chakladar et al., Biochem Biophys Res Commun 2005
:
Synergistic activation of the murine gastrin promoter by oncogenic Ras and
beta-catenin involves
SMAD recruitment
Jian et al., Genes Dev 2006
:
Smad3 dependent nuclear translocation of
beta-catenin is required for TGF-beta1 induced proliferation of bone marrow derived adult human mesenchymal stem cells ... We show that TGF-beta1 induces rapid nuclear translocation of
beta-catenin in MSCs in a
Smad3 dependent manner
Han et al., Dev Cell 2006
:
Further analysis revealed that independent of its role in
anti-Smad signaling, Smad7 bound beta-catenin and
induced beta-catenin degradation by recruiting an E3 ligase, Smurf2, to the Smad7/beta-catenin complex
Zhang et al., J Biol Chem 2007
:
Inhibition of
beta-catenin expression by small interfering RNA
augmented Smad3 signaling ... Inhibition of
beta-catenin in this cell line by small interfering RNA
resulted in increased TGF-beta1 dependent
Smad3 phosphorylation and restoration of TGF-beta1 anti-proliferative effects
Yang et al., Bone 2009
:
Both activated or total nuclear
Smad158 and Smad2 levels increase as they become confluent, and
beta-catenin protein expression
increases as 2T3 cells become confluent, reflecting a set of genes involved in early preosteoblast to osteoblast commitment, as observed in vitro and in vivo
Inoue et al., J Cell Biochem 2009
:
Role of
Smad3 ,
acting independently of transforming growth factor-beta, in the early induction of
Wnt-beta-catenin signaling by parathyroid hormone in mouse osteoblastic cells ... Transient transfection of
Smad3AAVA inhibited the PTH induction of total
beta-catenin and reduction of phosphorylated beta-catenin levels at 6 and 24 h, but not at 1 h, indicating that the early effects occur independently of TGF-beta receptor signaling
Zhang et al., J Biol Chem 2010
:
Smad3 prevents
beta-catenin degradation and facilitates beta-catenin nuclear translocation in chondrocytes ... Both
Smad3 and Smad4 were
required for the interaction with
beta-catenin and protected beta-catenin from an ubiquitin-proteasome dependent degradation