Characterization of deletions in the LDL receptor gene in patients with familial hypercholesterolemia in the United Kingdom.
Author(s) -
XiMing Sun,
Joe Webb,
Vilmundur Guðnason,
Steve E. Humphries,
Mary Seed,
Gilbert R. Thompson,
Brian L. Knight,
Anne K. Soutar
Publication year - 1992
Publication title -
arteriosclerosis and thrombosis a journal of vascular biology
Language(s) - English
Resource type - Journals
eISSN - 2330-9199
pISSN - 1049-8834
DOI - 10.1161/01.atv.12.7.762
Subject(s) - familial hypercholesterolemia , allele , genetics , southern blot , gene , gene duplication , exon , ldl receptor , biology , restriction fragment length polymorphism , mutation , allele frequency , microbiology and biotechnology , compound heterozygosity , genomic dna , mutant , population , lipoprotein , genotype , medicine , endocrinology , cholesterol , environmental health
A sample of 200 patients with a clinical diagnosis of heterozygous (189) or homozygous (11) familial hypercholesterolemia (FH) attending lipid clinics in the London area have been screened for the presence of major gene defects in the low density lipoprotein (LDL) receptor gene by Southern blotting of genomic DNA with specific probes. This study is part of a project to determine the frequency of known mutations in the LDL receptor gene in this population. A new polymorphism for the enzyme Bgl II was identified by hybridization with a probe specific for the promoter plus exon 1 of the LDL receptor gene. The observed frequency of the rare allele, characterized by a Bgl II fragment of 13 kb compared with 10 kb for the common allele, was 0.08 in this group of FH patients. Several individuals who were heterozygous for the rare allele were also heterozygous for a mutation elsewhere in the LDL receptor gene that is known to cause FH. Eight different mutations, seven deletions and one duplication, were detected in a total of nine patients, accounting for 4.5% of the mutant alleles in this group. Three of the mutations are apparently identical to deletions that have been described previously in FH patients of British or European origin, while the remaining five have not been described. Two of these were in patients of Polish and Asian Indian origin, while the other three were in patients of apparently British ancestry.
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