DESCRIPTION:

QTL associated with atherosclerosis 9. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (176558864)

LABEL:

QTL-Ath9-Mouse-Chr 1

SCORE TYPE:

Binary

DATE ADDED:

2012-04-02

DATE UPDATED:

2020-05-06

SPECIES:

URI:

http://www.informatics.jax.org/searches/accession_report.cgi?id=MGI:1890350

AUTHORS:

Dansky HM, Shu P, Donavan M, Montagno J, Nagle DL, Smutko JS, Roy N, Whiteing S, Barrios J, McBride TJ, Smith JD, Duyk G, Breslow JL, Moore KJ

TITLE:

A phenotype-sensitizing Apoe-deficient genetic background reveals novel atherosclerosis predisposition loci in the mouse.

JOURNAL:

Genetics Apr 2002, Vol 160, pp. 1599-608

ABSTRACT:

Therapeutic intervention for atherosclerosis has predominantly concentrated on regulating cholesterol levels; however, these therapeutics are not efficacious for all patients, suggesting that other factors are involved. This study was initiated to identify mechanisms that regulate atherosclerosis predisposition in mice other than cholesterol level regulation. To do so we performed quantitative trait locus analysis using two inbred strains that each carry the atherosclerosis phenotype-sensitizing Apoe deficiency and that have been shown to have widely disparate predilection to atherosclerotic lesion formation. One highly significant locus on chromosome 10 (LOD = 7.8) accounted for 19% of the variance in lesion area independent of cholesterol. Two additional suggestive loci were identified on chromosomes 14 (LOD = 3.2) and 19 (LOD = 3.2), each accounting for 7-8% of the lesion variance. In all, five statistically significant and suggestive loci affecting lesion size but not lipoprotein levels were identified. Many of these were recapitulated in an independent confirmatory cross. In summary, two independently performed crosses between C57BL/6 and FVB/N Apoe-deficient mice have revealed several previously unreported atherosclerosis susceptibility loci that are distinct from loci linked to lipoprotein levels. PUBMED: 11973313
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