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MADR2 maps to 18q21 and encodes a TGFbeta-regulated MAD-related protein that is functionally mutated in colorectal carcinoma.
Eppert, K; Scherer, S W; Ozcelik, H; Pirone, R; Hoodless, P; Kim, H; Tsui, L C; Bapat, B; Gallinger, S; Andrulis, I L; Thomsen, G H; Wrana, J L; Attisano, L.
Afiliación
  • Eppert K; Division of Gastroenterology, The Hospital for Sick Children, Toronto, Ontario, Canada.
Cell ; 86(4): 543-52, 1996 Aug 23.
Article en En | MEDLINE | ID: mdl-8752209
The MAD-related (MADR) family of proteins are essential components in the signaling pathways of serine/threonine kinase receptors for the transforming growth factor beta (TGFbeta) superfamily. We demonstrate that MADR2 is specifically regulated by TGFbeta and not bone morphogenetic proteins. The gene for MADR2 was found to reside on chromosome 18q21, near DPC4, another MADR protein implicated in pancreatic cancer. Mutational analysis of MADR2 in sporadic tumors identified four missense mutations in colorectal carcinomas, two of which display a loss of heterozygosity. Biochemical and functional analysis of three of these demonstrates that the mutations are inactivating. These findings suggest that MADR2 is a tumor suppressor and that mutations acquired in colorectal carcinomas may function to disrupt TGFbeta signaling.
Asunto(s)
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fosfoproteínas / Cromosomas Humanos Par 18 / Neoplasias Colorrectales / Transactivadores / Genes Supresores de Tumor / Factor de Crecimiento Transformador beta / Proteínas de Unión al ADN Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Cell Año: 1996 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Estados Unidos
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fosfoproteínas / Cromosomas Humanos Par 18 / Neoplasias Colorrectales / Transactivadores / Genes Supresores de Tumor / Factor de Crecimiento Transformador beta / Proteínas de Unión al ADN Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Cell Año: 1996 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Estados Unidos