Gene interactions and pathways from curated databases and text-mining

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CTNNB1 — TCF7L2

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

Shih et al., Cancer Res 2000 (Colorectal Neoplasms) : When expressed in colon cancer cells, Ad-CBR blocked the nuclear translocation of beta-catenin and inhibited beta-catenin/Tcf-4 mediated transactivation
Ogino et al., J Biol Chem 2001 : Bipartite binding of a kinase activator activates Cdc7 related kinase essential for S phase
Song et al., Mol Cell Biol 2003 : We also demonstrated cross talk between the WNT and androgen receptor signaling pathways because excess androgen receptor could interfere with WNT signaling and excess TCF-4 inhibited the interaction of beta-catenin and androgen receptor
Yamamoto et al., EMBO J 2003 : PIASy enhanced beta-catenin dependent transcriptional activity of Tcf-4 , whereas Axam inhibited it ... Furthermore, beta-catenin and PIASy activated Tcf-4 ( K297R ), in which Lys297 was changed to arginine, less than wild-type Tcf-4
Nath et al., Proc Natl Acad Sci U S A 2003 (Colonic Neoplasms) : We determined Beta-catenin dependent TCF-4 transcriptional activity by measuring the activity of the luciferase gene placed under the control of TCF-4 regulatory sequences
Alvarado et al., Genetics 2004 : Bipartite inhibition of Drosophila epidermal growth factor receptor by the extracellular and transmembrane domains of Kekkon1
Kanda et al., J Cell Biochem 2005 : Association with beta-catenin enhances the transcriptional activity of T-cell factor-4 (TCF-4) , which up-regulates the expression of fibronectin
Chi et al., Genes Dev 2007 : Bipartite stimulatory action of the Hop2-Mnd1 complex on the Rad51 recombinase
Lim et al., Cancer Res 2008 : Moreover, HIF-1alpha disruption of hARD1/beta-catenin repressed TCF4 activity, resulting in c-Myc suppression and p21 ( cip1 ) induction
Feng et al., J Physiol 2009 (Atrophy) : Based on these findings, the loss of EC proliferation with TPN may well be due to a loss of total beta-catenin, as well as a concomitant change in the differential expression of beta-catenin phosphorylation sites, and a reduction in beta-catenin mediated tcf-4 transcription
Huang et al., Biochem Biophys Res Commun 2009 : Constitutive activation of the transcription factor TCF4 activity by mutated APC or beta-catenin contributes to cell neoplastic transformation
Kaur et al., Neoplasia (New York, N.Y.) 2010 (Colorectal Neoplasms) : Other studies, therefore, were performed only in SW480 cells where silibinin significantly decreased beta-catenin dependent T-cell factor-4 (TCF-4) transcriptional activity and protein expression of beta-catenin target genes such as c-Myc and cyclin D1
Thévenod et al., Curr Mol Med 2010 (Kidney Neoplasms...) : Wnt signaling may contribute to Cd2+ carcinogenesis because Cd2+ disrupts the junctional E-cadherin/beta-catenin complex, resulting in excessive nuclear translocation of beta-catenin and activation of Tcf4