A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Evidence for linkage to and association with type 1 diabetes at the 3q21 region in the Finnish population
Tekijät: Laine AP, Turpeinen H, Veijola R, Hermann R, Simell O, Knip M, Ilonen J
Kustantaja: NATURE PUBLISHING GROUP
Julkaisuvuosi: 2006
Journal: Genes and Immunity
Tietokannassa oleva lehden nimi: GENES AND IMMUNITY
Lehden akronyymi: GENES IMMUN
Vuosikerta: 7
Numero: 1
Aloitussivu: 69
Lopetussivu: 72
Sivujen määrä: 4
ISSN: 1466-4879
DOI: https://doi.org/10.1038/sj.gene.6364269
Tiivistelmä
IDDM9-region on chromosome 3q has shown suggestive evidence for linkage to type 1 diabetes in some but not all genome scans. We analyzed 22 microsatellite markers in 121 Finnish type 1 diabetes multiplex families across the IDDM9-region. Two-point maximum LOD scores of 3.4 and 2.5 were detected with markers D3S1589 and D3S3606, respectively. Two markers were further tested for association using the transmission disequilibrium test in 384 Finnish type 1 diabetes simplex families. Marker AFM203wd10 showed association with type 1 diabetes ( P = 0.0002 for allele R16). Association was present in families with children carrying the HphI-23 AA risk genotype at IDDM2 but not in families with children carrying protective AT or TT genotypes implying interaction between the two loci. Our data gives credence to earlier findings of linkage in this region and suggests a location for a polymorphism affecting type 1 diabetes susceptibility in the area surrounding AFM203wd10.
IDDM9-region on chromosome 3q has shown suggestive evidence for linkage to type 1 diabetes in some but not all genome scans. We analyzed 22 microsatellite markers in 121 Finnish type 1 diabetes multiplex families across the IDDM9-region. Two-point maximum LOD scores of 3.4 and 2.5 were detected with markers D3S1589 and D3S3606, respectively. Two markers were further tested for association using the transmission disequilibrium test in 384 Finnish type 1 diabetes simplex families. Marker AFM203wd10 showed association with type 1 diabetes ( P = 0.0002 for allele R16). Association was present in families with children carrying the HphI-23 AA risk genotype at IDDM2 but not in families with children carrying protective AT or TT genotypes implying interaction between the two loci. Our data gives credence to earlier findings of linkage in this region and suggests a location for a polymorphism affecting type 1 diabetes susceptibility in the area surrounding AFM203wd10.
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