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WNT signaling pathway is implicated in carcinogenesis, embryogenesis and organogenesis. Gain-of-function mutations of positive regulators of the WNT-β-catenin pathway or loss-of-function mutations of negative regulators of the WNT-β-catenin pathway leads to carcinogenesis through transcriptional activation of WNT target genes. Because WNT signaling molecules are potent targets in the fields of oncology (diagnosis, prevention and treatment) and regenerative medicine (stem cell biology), we have so far cloned and characterized the following human genes encoding WNT signaling molecules: WNT2B/WNT13, WNT3, WNT3A, WNT5B, WNT6, WNT7B, WNT8A, WNT8B, WNT10A, WNT10B, WNT11, WNT14 and WNT14B/WNT15 among 19 WNT genes in the human genome, FZD1, FZD2, FZD3, FZD4, FZD5, FZD6, FZD7, FZD8 and FZD10 among 10 FZD genes in the human genome, and also FRAT1, FRAT2, NKD1, NKD2, VANGL1/STB2, ARHU/WRCH1, ARHV/WRCH2, GIPC2, GIPC3, βTRCP2/FBXW1B, SOX17, and TCF-3 genes. Genome-wide comprehensive expression analyses on WNT signaling molecules revealed that expression profile of WNT signaling molecules were dramatically changed during neuronal differentiation of NT2 cells, and also that some WNT signaling molecules, such as WNT2 and WNT5A, were up-regulated in primary gastric cancer due to cancer - stromal interaction. (Correspondence: Masaru Katoh) |
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Last Update:2004/12/01 contact |
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