Beta- and gamma-catenin mutations, but not E-cadherin inactivation, underlie T-cell factor/lymphoid enhancer factor transcriptional deregulation in gastric and pancreatic cancer.
Caca K, Kolligs FT, Ji X, Hayes M, Qian J, Yahanda A, Rimm DL, Costa J, Fearon ER. Beta- and gamma-catenin mutations, but not E-cadherin inactivation, underlie T-cell factor/lymphoid enhancer factor transcriptional deregulation in gastric and pancreatic cancer. Molecular Cancer Research 1999, 10: 369-76. PMID: 10392898.Peer-Reviewed Original ResearchMeSH KeywordsAdenomatous Polyposis Coli ProteinAmino Acid SequenceAnimalsBeta CateninCadherinsCytoskeletal ProteinsDesmoplakinsDNA-Binding ProteinsGamma CateninGene Expression Regulation, NeoplasticHMGB ProteinsHumansLymphoid Enhancer-Binding Factor 1Molecular Sequence DataMutagenesisPancreatic NeoplasmsStomach NeoplasmsTCF Transcription FactorsTrans-ActivatorsTranscription Factor 7-Like 1 ProteinTranscription FactorsTranscription, GeneticTumor Cells, CulturedConceptsPhosphorylation sitesMutant proteinsGlycogen synthase kinase 3beta phosphorylation sitesGlycogen synthase kinase-3betaFactor transcription factorsPotential phosphorylation sitesSynthase kinase-3betaTCF transcriptional activityE-cadherin inactivationNH2-terminal deletionsRole of APCImportant binding partnerSerine 28TCF transcriptionTranscriptional deregulationT-cell factorBinding partnerTranscription factorsAPC proteinKinase-3betaTranscriptional activityNH2 terminusAdenomatous polyposis coli (APC) mutationsCell adhesionPancreatic cancer lines