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Journal of Lipid Research, Vol 37, 1406-1421, Copyright © 1996 by Lipid Research, Inc.
CL Welch, YR Xia, I Shechter, R Farese, M Mehrabian, S Mehdizadeh, CH Warden and AJ Lusis
As part of an effort to dissect the genetic factors involved in cholesterol
homeostasis in the mouse model, we report the mapping of 12 new candidate
genes using linkage analysis. The genes include: cytoplasmic HMG-CoA
synthase (Hmgcs 1, Chr 13), mitochondrial synthase (Hmgcs 2, Chr 3), a
synthase-related sequence (Hmgcs 1-rs, Chr 12), mevalonate kinase (Mvk, Chr
5), farnesyl diphosphate synthase (Fdps, Chr 3), squalene synthase (Fdft 1,
Chr 14), acyl-CoA:cholesterol acyltransferase (Acact, Chr 1), sterol
regulatory element binding protein-1 (Srebf1, Chr 8) and -2 (Srebf2, Chr
15), apolipoprotein A-I regulatory protein (Tcfcoup2, Chr 7), low density
receptor-related protein-related sequence (Lrp-rs, Chr 10), and
Lrp-associated protein (Lrpap 1, Chr 5). In addition, the map positions for
several lipoprotein receptor genes were refined. These genes include: low
density lipoprotein receptor (Ldlr, Chr 9), very low density lipoprotein
receptor (Vldlr, Chr 19), and glycoprotein 330 (Gp330, Chr 2). Some of
these candidate genes are located within previously defined chromosomal
regions (quantitative trait loci, QTLs) contributing to plasma lipoprotein
levels, and Acact maps near a mouse mutation, ald, resulting in depletion
of cholesteryl esters in the adrenals. The combined use of QTL and
candidate gene mapping provides a powerful means of dissecting complex
traits such as cholesterol homeostasis.
ARTICLES
Genetic regulation of cholesterol homeostasis: chromosomal organization of candidate genes [published erratum appears in J Lipid Res 1996 Oct;37(10):2269]
Department of Pathology, University of California, Los Angeles 90095, USA.
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