Mutation analysis in familial hypercholesterolemia patients of different ancestries: identification of three novel LDLR gene mutations

Mol Cell Probes. 1998 Jun;12(3):149-52. doi: 10.1006/mcpr.1998.0164.

Abstract

Twelve familial hypercholesterolemia (FH) patients of different ancestries living in South Africa were subjected to mutation analysis of the low-density lipoprotein receptor (LDLR) gene. Nine different mutations were identified in 10 patients. Six of these, including the founder-related mutation C660X identified in two Lebanese patients, have previously been described in other FH patients with compatible genetic backgrounds, and/or in patients originating from countries where admixture is not uncommon. Characterization of an abnormal electrophoresis pattern detected in exon 4 of the LDLR gene by heteroduplex single-strand conformation polymorphism (HEX-SSCP) analysis, revealed a novel G deletion at codon 185 (617delG) which resulted in a downstream stop codon. Two of the new mutations identified resulted in amino acid substitutions and were designated R57C and Q357P.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apolipoproteins B / genetics
  • Base Sequence
  • DNA Mutational Analysis
  • Ethnicity / genetics
  • Exons
  • Humans
  • Hyperlipoproteinemia Type II / genetics*
  • Point Mutation*
  • Polymerase Chain Reaction / methods
  • Polymorphism, Single-Stranded Conformational
  • Receptors, LDL / genetics*
  • Sequence Deletion*
  • South Africa

Substances

  • Apolipoproteins B
  • Receptors, LDL