Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
GENETIC-STRUCTURE OF 5 SUSCEPTIBILITY GENE REGIONS FOR CORONARY-ARTERY DISEASE - DISEQUILIBRIA WITHIN AND AMONG REGIONS
Autore:
ZERBA KE; FERRELL RE; SING CF;
Indirizzi:
COLGATE UNIV,DEPT BIOL,13 OAK DR HAMILTON NY 13346 UNIV PITTSBURGH,DEPT HUMAN GENET PITTSBURGH PA 15262 UNIV MICHIGAN,DEPT HUMAN GENET ANN ARBOR MI 48109
Titolo Testata:
Human genetics
fascicolo: 3, volume: 103, anno: 1998,
pagine: 346 - 354
SICI:
0340-6717(1998)103:3<346:GO5SGR>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
LDL RECEPTOR GENE; APOLIPOPROTEIN-E POLYMORPHISM; GENOTYPE-PHENOTYPE RELATIONSHIPS; LIPOPROTEIN-LIPASE GENE; POPULATION-BASED SAMPLE; LINKAGE DISEQUILIBRIUM; CLADISTIC-ANALYSIS; GAMETIC DISEQUILIBRIUM; B GENE; PHYSICAL DISTANCE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
90
Recensione:
Indirizzi per estratti:
Citazione:
K.E. Zerba et al., "GENETIC-STRUCTURE OF 5 SUSCEPTIBILITY GENE REGIONS FOR CORONARY-ARTERY DISEASE - DISEQUILIBRIA WITHIN AND AMONG REGIONS", Human genetics, 103(3), 1998, pp. 346-354

Abstract

We analyzed two-locus disequilibria for 16 polymorphic loci of seven susceptibility genes for coronary artery disease located in five chromosomal regions distributed across four chromosomes. Included were the genes coding for apolipoprotein B (ApoB, chromosome 2, four marker loci), lipoprotein lipase (LPL, chromosome 8, three marker loci), apolipoproteins AI, CIII, AIV (Apo-AI-CIII-AIV, chromosome 11, three marker loci), apolipoprotein E (ApoE, chromosome 19, two marker loci), and thelow density lipoprotein receptor (LDLR, chromosome 19, four marker loci). Our sample included 540 unrelated individuals from the Rochester,Minn. population, There were no statistically significant deviations of single-locus genotypes from Hardy-Weinberg equilibrium. The strongest associations within genes were for composite diallelic disequilibria; 17/19 were significant (13 at Pr <0.001, 1 at Pr <0.01, 3 at Pr <0.05). These observations suggest marker alleles within genes have a shared evolutionary history reflected by disequilibria that have not beendissipated by recombination. Disequilibrium was not generally concordant with the physical orderings of markers. Only two significant higher-order disequilibria were observed although 12 triallelic disequilibria were at maximum possible values. We observed 19 statistically significant disequilibria (Pr <0.05; 4 composite diallelic, 13 triallelic, and 2 quadriallelic) between 101 pairs of marker loci, where each locus in a pair was from a different unlinked region. These unexpected results are most likely explained by recent historical factors, includingworldwide population expansion and amalgamation with continuous admixture, that influence the genetic structure (organization of alleles and non-alleles into genotypes) of a population. We conclude that disequilibria between loci from unlinked regions may be more extensive than is commonly assumed. Our findings also suggest that it is, on average,at least 15 times more likely to not detect significant disequilibrium among unlinked loci when it is really present than to make a false positive inference. Disequilibria between functional loci within or between regions will impact estimates of genetic variance associated withparticular functional mutations within a susceptibility gene region.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 11:37:22