A quantitative protein S deficiency associated with a novel nonsense mutation and markedly reduced levels of mutated mRNA

Thromb Haemost. 1995 Aug;74(2):590-5.

Abstract

A 50-year-old Japanese man who had experienced recurrent episodes of venous thrombosis was found to have a hereditary protein S deficiency. The amount of total protein S antigen in plasma was reduced by approximately 50% in the patient and his two sons. DNA sequence analysis revealed a novel nonsense mutation, TAG for Gln 522 (CAG), in exon 14 of the protein S gene. Family studies performed by mutagenic PCR followed by restriction enzyme digestion showed that the proband and his two sons were heterozygous for this mutation. An mRNA-based analysis indicated that transcripts of the mutated allele were markedly reduced in the platelets of the affected individuals. Immunoblot analysis failed to detect the truncated mutant of protein S in the plasma or platelets of affected members. Our results demonstrated that this novel nonsense mutation was responsible for the quantitative deficiency of protein S.

Publication types

  • Case Reports

MeSH terms

  • Amino Acid Sequence
  • Base Sequence
  • Blood Platelets / chemistry
  • Complement Inactivator Proteins*
  • DNA Mutational Analysis
  • Female
  • Genetic Predisposition to Disease
  • Glycoproteins*
  • Humans
  • Male
  • Middle Aged
  • Molecular Sequence Data
  • Pedigree
  • Point Mutation
  • Polymerase Chain Reaction
  • Protein S / genetics*
  • Protein S Deficiency / complications
  • Protein S Deficiency / genetics*
  • RNA, Messenger / blood
  • RNA, Messenger / genetics*
  • Receptors, Complement / analysis
  • Recurrence
  • Thrombophlebitis / genetics*
  • Thrombophlebitis / prevention & control
  • Warfarin / therapeutic use

Substances

  • Complement Inactivator Proteins
  • Glycoproteins
  • Protein S
  • RNA, Messenger
  • Receptors, Complement
  • Warfarin