A new case of apo C-II deficiency with a nonsense mutation in the apo C-II gene

Clin Chim Acta. 1994 Jan 31;224(2):111-8. doi: 10.1016/0009-8981(94)90176-7.

Abstract

The apo C-II gene from a patient with apo C-II deficiency has been sequenced after amplification by the polymerase chain reaction (PCR). The sequence analysis revealed a substitution of adenosine for cytosine at position 3,002 in exon 3, leading to the introduction of a premature stop codon (TAA) at a position corresponding to aminoacid 37 of mature apo C-II. This mutation creates a new Rsa I restriction enzyme site in the apo C-II gene. Amplification of DNA from family members by PCR and digestion with Rsa I established that the patient is a true homozygote for this mutation. The same nucleotide has been substituted for the mutation apo C-IIPadova and apo C-IIBari previously described in two kindreds from Italy. From these data we speculate that base pair 3,002 in the apo C-II gene may represent a hot spot for mutation.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apolipoprotein C-II
  • Apolipoproteins C / deficiency*
  • Apolipoproteins C / genetics*
  • Base Sequence
  • Child, Preschool
  • Cholesterol / blood
  • Exons / physiology
  • Humans
  • Hyperlipoproteinemia Type II / genetics
  • Isoelectric Focusing
  • Lipoprotein Lipase / blood
  • Male
  • Molecular Sequence Data
  • Mutation
  • Polymerase Chain Reaction
  • Sequence Analysis, DNA
  • Triglycerides / blood

Substances

  • Apolipoprotein C-II
  • Apolipoproteins C
  • Triglycerides
  • Cholesterol
  • Lipoprotein Lipase