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Expression of -Catenin, a Key Mediator of the WNT Signaling Pathway, in Basal Cell Carcinoma

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Inactivation of the patched (PTCH) gene seems to be responsible for the genesis of basal cell carcinoma (BCC). The PTCH protein forms a complex with another membrane-bound molecule, smoothened (SMO), and is an important component in the SMO/hedgehog signaling pathway.¹ Binding of PTCH to SMO represses the SMO signaling pathway, but when hedgehog is bound to PTCH, the PTCH protein seems to undergo a conformational change that leads to activation of the SMO pathway. Activation can also occur if PTCH is inactivated by loss of heterozygosity and/or mutation. Activation of the pathway results in transcription of downstream target genes. These targets may include members of the transforming growth factor , bone morphologic protein, and WNT protein families, as well as PTCH itself.²

-Catenin is a multifunctional protein that plays a role in both cell adhesion and gene transcription. The role of -catenin in adhesion has been well established . . . [Full Text of this Article]

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

G-Protein-Coupled Receptor GPR49 is Up-regulated in Basal Cell Carcinoma and Promotes Cell Proliferation and Tumor Formation
Tanese et al.
Am. J. Pathol. 2008;173:835-843.
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