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dc.contributor.advisorÖztürk, M.en_US
dc.contributor.authorÇağatay, T.en_US
dc.date.accessioned2016-07-01T10:55:39Z
dc.date.available2016-07-01T10:55:39Z
dc.date.issued2002
dc.identifier.urihttp://hdl.handle.net/11693/29206
dc.descriptionCataloged from PDF version of article.en_US
dc.description.abstractβ-catenin is involved in both cell-cell interactions and wnt pathway-dependent cell fate determination through its interactions with E-cadherin and TCF/LEF transcription factors, respectively. Cytoplasmic/nuclear levels of β-catenin are important in regulated transcriptional activation of TCF/LEF target genes. Normally, these levels are kept low by proteosomal degradation of â-catenin through Axin1- and APC-dependent phosphorylation by CKI and GSK-3β. Deregulation of β-catenin degradation results in its aberrant accumulation, often leading to cancer. Accordingly, aberrant accumulation of β-catenin is onberved at high frequency in many cancers. This accumulation correlates with either mutational activation of CTNNB1 (β-catenin) or mutational inactivation of APC and Axin1 genes in some tumors. However, there are many tumors that display β-catenin accumulation in the absence of a mutation in these genes. Thus, there must be additional sources for aberrant β-catenin accumulation in cancer cells. Here, we provide experimental evidence that wild-type β-catenin accumulates in hepatocellular carcinoma (HCC) cells in association with mutational inactivation of p53 gene. We also show that worldwide p53 and β-catenin mutation rates are inversely correlated in HCC. These data suggest that inactivation of p53 is an important cause of aberrant accumulation of β−catenin in cancer cells.en_US
dc.description.statementofresponsibilityÇağatay, Tolgaen_US
dc.format.extentxviii, 157 leaves, illustrations, 30 cmen_US
dc.language.isoEnglishen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subject.lccQZ202 .C34 2002en_US
dc.subject.lcshp53 antioncogene.en_US
dc.titlep53 mutations as a source of aberrant Beta-catenin accumulation in cancer cellsen_US
dc.typeThesisen_US
dc.departmentDepartment of Moleculer Biology and Geneticsen_US
dc.publisherBilkent Universityen_US
dc.description.degreePh.D.en_US
dc.identifier.itemidBILKUTUPB040649


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