Type 2 Diabetes Whole-Genome Association Study in Four Populations: The DiaGen Consortium
Type 2 diabetes (T2D) is a common, polygenic chronic disease with high heritability. The purpose of this whole-genome association study was to discover novel T2D-associated genes. We genotyped 500 familial cases and 497 controls with >300,000 HapMap-derived tagging single-nucleotide–polymorphism...
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creator | Salonen, Jukka T. Uimari, Pekka Aalto, Juha-Matti Pirskanen, Mia Kaikkonen, Jari Todorova, Boryana Hyppönen, Jelena Korhonen, Veli-Pekka Asikainen, Janne Devine, Christopher Tuomainen, Tomi-Pekka Luedemann, Jan Nauck, Matthias Kerner, Wolfgang Stephens, Richard H. New, John P. Ollier, William E. Gibson, J. Martin Payton, Antony Horan, Michael A. Pendleton, Neil Mahoney, Walt Meyre, David Delplanque, Jerôme Froguel, Philippe Luzzatto, Oren Yakir, Benjamin Darvasi, Ariel |
description | Type 2 diabetes (T2D) is a common, polygenic chronic disease with high heritability. The purpose of this whole-genome association study was to discover novel T2D-associated genes. We genotyped 500 familial cases and 497 controls with >300,000 HapMap-derived tagging single-nucleotide–polymorphism (SNP) markers. When a stringent statistical correction for multiple testing was used, the only significant SNP was at
TCF7L2, which has already been discovered and confirmed as a T2D-susceptibility gene. For a replication study, we selected 10 SNPs in six chromosomal regions with the strongest association (singly or as part of a haplotype) for retesting in an independent case-control set including 2,573 T2D cases and 2,776 controls. The most significant replicated result was found at the
AHI1-LOC441171 gene region. |
doi_str_mv | 10.1086/520599 |
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TCF7L2, which has already been discovered and confirmed as a T2D-susceptibility gene. For a replication study, we selected 10 SNPs in six chromosomal regions with the strongest association (singly or as part of a haplotype) for retesting in an independent case-control set including 2,573 T2D cases and 2,776 controls. The most significant replicated result was found at the
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TCF7L2, which has already been discovered and confirmed as a T2D-susceptibility gene. For a replication study, we selected 10 SNPs in six chromosomal regions with the strongest association (singly or as part of a haplotype) for retesting in an independent case-control set including 2,573 T2D cases and 2,776 controls. The most significant replicated result was found at the
AHI1-LOC441171 gene region.</description><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Vesicular Transport</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Chromosomes</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>England</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Finland</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Frequency</subject><subject>General aspects. Genetic counseling</subject><subject>Genes</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetics</subject><subject>Genetics of eukaryotes. Biological and molecular evolution</subject><subject>Genome, Human</subject><subject>Genomics</subject><subject>Genotype & phenotype</subject><subject>Germany</subject><subject>Human genetics</subject><subject>Humans</subject><subject>Israel</subject><subject>Jews - genetics</subject><subject>Life Sciences</subject><subject>Linkage Disequilibrium</subject><subject>Male</subject><subject>Medical genetics</subject><subject>Medical sciences</subject><subject>Molecular and cellular biology</subject><subject>Polymorphism, Single Nucleotide</subject><subject>White People</subject><issn>0002-9297</issn><issn>1537-6605</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU-LE0EQxRtR3LjqR5BGUPAw2jWT_udBCFl3VwgoGBFPTaenxvQyMx27ZwL59tsxwWgungqqfvWqeI-Q58DeAlPiHS8Z1_oBmQCvZCEE4w_JhDFWFrrU8oI8SemOMQDFqsfkAqQQqlLlhPxY7jZIS3rl7QoHTPT7OrRY3GAfOqSzlILzdvChp1-Hsd5R39PrMEb6JWzG9vcgvafLNe4F8hKd50aIgx-7p-RRY9uEz471kny7_ric3xaLzzef5rNF4biuhqIRvNayks2q0QjKCSURnbYMrMWpUtI6MQXGXbNyUycaUTuAquaNqxQHqapL8uGguxlXHdYO-yHa1myi72zcmWC9-XfS-7X5GbYGNGcKdBZ4cxBYn63dzhZm38u-yVILsYXMvj4ei-HXiGkwnU8O29b2GMZkhAImFef_BUErDVxWGXx5Bt5lf_vsmClBC6anQp_UXAwpRWz-_AnM7PM3h_wz-OJvM07YMfAMvDoCNjnbNtH2zqcTp3IWGvYcO3CYo9t6jCY5j73D2kd0g6mDP799Dy1ixkY</recordid><startdate>20070801</startdate><enddate>20070801</enddate><creator>Salonen, Jukka T.</creator><creator>Uimari, Pekka</creator><creator>Aalto, Juha-Matti</creator><creator>Pirskanen, Mia</creator><creator>Kaikkonen, Jari</creator><creator>Todorova, Boryana</creator><creator>Hyppönen, Jelena</creator><creator>Korhonen, Veli-Pekka</creator><creator>Asikainen, Janne</creator><creator>Devine, Christopher</creator><creator>Tuomainen, Tomi-Pekka</creator><creator>Luedemann, Jan</creator><creator>Nauck, Matthias</creator><creator>Kerner, Wolfgang</creator><creator>Stephens, Richard H.</creator><creator>New, John P.</creator><creator>Ollier, William E.</creator><creator>Gibson, J. 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We genotyped 500 familial cases and 497 controls with >300,000 HapMap-derived tagging single-nucleotide–polymorphism (SNP) markers. When a stringent statistical correction for multiple testing was used, the only significant SNP was at
TCF7L2, which has already been discovered and confirmed as a T2D-susceptibility gene. For a replication study, we selected 10 SNPs in six chromosomal regions with the strongest association (singly or as part of a haplotype) for retesting in an independent case-control set including 2,573 T2D cases and 2,776 controls. The most significant replicated result was found at the
AHI1-LOC441171 gene region.</abstract><cop>Chicago, IL</cop><pub>Elsevier Inc</pub><pmid>17668382</pmid><doi>10.1086/520599</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-4850-7444</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Vesicular Transport Biological and medical sciences Case-Control Studies Chromosomes Diabetes Diabetes Mellitus, Type 2 - genetics Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies England Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Finland Fundamental and applied biological sciences. Psychology Gene Frequency General aspects. Genetic counseling Genes Genetic Predisposition to Disease Genetics Genetics of eukaryotes. Biological and molecular evolution Genome, Human Genomics Genotype & phenotype Germany Human genetics Humans Israel Jews - genetics Life Sciences Linkage Disequilibrium Male Medical genetics Medical sciences Molecular and cellular biology Polymorphism, Single Nucleotide White People |
title | Type 2 Diabetes Whole-Genome Association Study in Four Populations: The DiaGen Consortium |
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