Fine mapping of Hyplip1 and the human homolog, a potential locus for FCHL |
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Authors: | Päivi Pajukanta Jackie S Bodnar Riitta Sallinen Michael Chu Tuula Airaksinen Qunong Xiao Lawrence W Castellani Sonal S Sheth Maija Wessman Aarno Palotie Janet S Sinsheimer Peter Demant Aldons J Lusis Leena Peltonen |
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Institution: | (1) UCLA, Department of Human Genetics, Gonda Neuroscience and Genetics Research Center, 695 Charles E. Young Drive South, Box 708822, Los Angeles, California 90095-7088, USA, US;(2) Department of Medicine, Department of Microbiology and Molecular Genetics, and Molecular Biology Institute, University of California, Los Angeles, California, USA, US;(3) Department of Clinical Chemistry, Helsinki University Central Hospital, Finland, FI;(4) Department of Biosciences, Division of Genetics, University of Helsinki, Finland, FI;(5) Department of Biomathematics, University of California, Los Angeles, California, USA, US;(6) Division of Molecular Genetics, The Netherlands Cancer Institute, Amsterdam, The Netherlands, NL |
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Abstract: | Familial combined hyperlipidemia (FCHL) is a common genetic dyslipidemia predisposing to premature coronary heart disease
(CHD). We previously identified a locus for FCHL on human Chromosome (Chr) 1q21-q23 in 31 Finnish FCHL families. We also mapped
a gene for combined hyperlipidemia (Hyplip1) to a potentially orthologous region of mouse Chr 3 in the HcB-19/Dem mouse model of FCHL. The human FCHL locus was, however, originally mapped about 5 Mb telomeric to the synteny border, the
centromeric part of which is homologous to mouse Chr 3 and the telomeric part to mouse Chr 1. To further localize the human
Hyplip1 homolog and estimate its distance from the peak linkage markers, we fine-mapped the Hyplip1 locus and defined the borders of the region of conserved synteny between human and mouse. This involved establishing a physical
map of a bacterial artificial chromosome (BAC) contig across the Hyplip1 locus and hybridizing a set of BACs to both human and mouse chromosomes by fluorescence in situ hybridization (FISH). We
narrowed the location of the mouse Hyplip1 gene to a 1.5-cM region that is homologous only with human 1q21 and within approximately 5–10 Mb of the peak marker for linkage
to FCHL. FCHL is a complex disorder and this distance may, thus, reflect the well-known problems hampering the mapping of
complex disorders. Further studies identifying and sequencing the Hyplip1 gene will show whether the same gene predisposes to hyperlipidemia in human and mouse.
Received: 9 September 2000 / Accepted: 30 October 2000 |
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