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