Gene interactions and pathways from curated databases and text-mining

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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 *

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