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CTNNB1 — TP53

Text-mined interactions from Literome

Damalas et al., EMBO J 1999 (Colorectal Neoplasms) : Excess beta-catenin promotes accumulation of transcriptionally active p53 ... To examine whether these two key steps in carcinogenesis are interrelated, we studied the effect of excess beta-catenin on p53
Sadot et al., Mol Cell Biol 2001 : The inhibitory effect of p53 on beta-catenin is apparently mediated by the ubiquitin-proteasome system and requires an active glycogen synthase kinase 3beta ( GSK3beta )
Oren et al., Biochem Pharmacol 2002 (Neoplasms) : Whereas deregulated beta catenin can lead to Mdm2 inactivation and p53 accumulation, active p53 can promote the degradation and downregulation of beta catenin
Oren et al., Ann N Y Acad Sci 2002 (Neoplasms) : Whereas deregulated beta-catenin can lead to Mdm2 inactivation and p53 accumulation, active p53 can promote the degradation and down-regulation of beta-catenin
Sills et al., Carcinogenesis 2004 (Cecal Neoplasms...) : Using immunohistochemistry beta-catenin ( encoded by Catnb ) protein accumulation was detected in 80 % ( 8/10 ) of the cecal carcinomas, while increased cyclin D1 and p53 protein expression was detected in 73 % ( 8/11 ), respectively
Levina et al., Oncogene 2004 : Deregulated beta-catenin can cause the activation of p53 , a key tumor suppressor mutated in most cancers ... We found that the p53 mediated reduction in beta-catenin involves enhanced phosphorylation of beta-catenin on key NH ( 2 ) -terminal serines and requires CK1 and GSK-3beta activities, both being components of the beta-catenin degradation machinery ... p53 also induced a shift in the distribution of the scaffold molecule Axin to a Triton X-100-soluble fraction, and led to depletion of beta-catenin from this Triton-soluble fraction
Chung et al., Cancer 2004 (Breast Neoplasms) : Recently, it was shown that p53 down-regulated beta-catenin in a complex fashion
Iwai et al., Oncogene 2004 : Siah-1L, a novel transcript variant belonging to the human Siah family of proteins, regulates beta-catenin activity in a p53 dependent manner
Fukushima et al., Immunity 2006 : Previously, we discovered a novel pathway for p53 induced beta-catenin degradation through a ubiquitin E3 ligase complex involving Siah1, SIP ( CacyBP ), Skp1, and Ebi
Ji et al., Oncogene 2007 : Additionally, Gadd45a facilitates ultraviolet radiation induced degradation of cytoplasmic and nuclear beta-catenin in a p53 dependent manner via activation of p38 kinase
Jung et al., J Gen Virol 2007 (Carcinoma, Hepatocellular...) : In the presence of p53 , HBx downregulated beta-catenin through the activation of a p53-Siah-1 proteasome pathway
Iwai et al., Oncogene 2008 : Here, we show that human coiled-coil domain containing 85B ( CCDC85B ) is induced by p53 and regulates beta-catenin activity via interaction with the T-cell factor 4 in the nucleus ... In conclusion, we revealed that CCDC85B induced degradation of beta-catenin is independent of GSK3beta and other p53-inducible products, Siah-1L, suggesting that CCDC85B constitutes the one of the frameworks of p53 induced multiple regulatory pathways for beta-catenin activity
Tseng et al., Oncogene 2008 (Carcinoma, Non-Small-Cell Lung...) : Therefore, we postulated that alteration of the degradation complex AXIN2 ( axis inhibition protein 2 ) and betaTrCP ( beta-transducin repeat containing protein ) and p53 regulation could result in beta-catenin protein accumulation in lung cancer
Momota et al., Oncogene 2008 (Disease Models, Animal...) : As elevated c-Myc expression, activation of Wnt/beta-catenin signaling and dysfunction of p53 are seen in human PNETs, we investigated what role these abnormalities have in the formation of PNETs
Zhai et al., J Histochem Cytochem 2008 (Neoplasms) : Although CacyBP/SIP was implicated in p53 induced beta-catenin degradation, its exact function was still unknown
Puca et al., J Exp Clin Cancer Res 2008 : The beta-catenin degradation was dependent on HIPK2 catalytic activity and independent of p53 and glycogen synthase kinase 3beta ( GSK-3beta ) activities