beta-catenin


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beta-catenin

A cell–cell adhesion protein that binds to the cytoplasmic domain of E-cadherin. The beta-catenin-cadherin complex recruits alpha-catenin, which in turn binds actin of the cytoskeleton, together forming intercellular adherens junction. Beta-catenin also acts as a component of the Wnt signal transduction pathway, which regulates cell proliferation and differentiation. Tissue concentrations of free beta-catenin are controlled by a protein complex (adenomatous polyposis coli protein and glycogen synthetase kinase3a) which facilitates its breakdown. Wnt inactivates glycogen synthetase kinase3b, allowing beta-catenin to accumulate in cytoplasm and in the nucleus, where it activates the TCF/LEF transcription factors, which in turn act on c-myc, tcf-1 and cyclin D1.

Normal expression
Normal cells show membrane staining for beta-catenin. Beta-catenin expression is regulated by the adenomatous polyposis coli (APC) gene.
 
Abnormal expression
Cytoplasmic and/or nuclear staining is abnormal. Mutant CTNNB1 can lead to stabilisation of beta-catenin in the cytoplasm and translocation to the nucleus; disregulation of beta-catenin occurs in Gardner syndrome, leading to familial adenomatous polyposis and fibromatosis. Beta-catenin expression is increased in aggressive fibromatosis, synovial sarcoma, osteosarcoma, liposarcoma and malignant fibrous histiocytoma. High nuclear expression is seen in some mesenchymal tumours; cytoplasmic staining is seen in many. In contrast, cytoplasmic accumulation of beta-catenin is a generally good prognostic marker in upper and lower GI adenocarcinomas.
References in periodicals archive ?
The relative mRNA expression levels of genes (DKK-1, beta-catenin, c-myc, cyclin D1, and survivin) were normalized to GAPDH, calculated by using the [2.sup.-[DELTA][DELTA]Ct] method.
Kaykas, "WNT and beta-catenin signalling: diseases and therapies," Nature Reviews.
Biotin-rich, optically clear nuclei express estrogen receptor-beta: tumors with morules may develop under the influence of estrogen and aberrant beta-catenin expression.
Thus, beta-catenin, GSK-3beta, and the ratio of phosphorylated/dephosphorylated GSK-3beta were detected to determine whether inhibiting the Wnt/beta-catenin signaling pathway is the key to induce MSCs differentiation into cardiomyocytes.
The microphthalmia-associated transcription factor Mitf interacts with beta-catenin to determine target gene expression.
Nuclear beta-catenin expression distinguishes deep fibromatosis from other benign and malignant fibroblastic and myofibroblastic lesions.
Expression of epithelial-cadherin, alpha-catenin and beta-catenin during human intrahepatic bile duct development: a possible role in bile duct morphogenesis.
Our data suggest that the broad spectrum of pharmacological action of Uncaria tomentosa involves inhibition of the Wnt-signaling pathway, downstream of beta-Catenin activity.
Beta-catenin, an inducer of uncontrolled cell proliferation and migration in malignancies, is localized in the cytoplasm of vascular endothelium during neovascularization after myocardial infarction.
In particular, most colorectal cancers are due to hyperactive Wnt pathway activity in the intestinal epithelium, caused by mutational inactivation of the Adenomatous Polyposis Coli (APC) tumour suppressor or by mutational activation of beta-catenin. Our aim is to understand the molecular and cell-biological events during Wnt signalling in normal and malignant cells.
Frecuent mutations of beta-catenin in mouse colon tumors induces by azoxymethane.
Biphenotypic sinonasal sarcoma: an expanded immunoprofile including consistent nuclear beta-catenin positivity and absence of SOX10 expression.