A basic transthyretin variant (Glu61-->Lys) causes familial amyloidotic polyneuropathy: protein and DNA sequencing and PCR-induced mutation restriction analysis

Biochem Biophys Res Commun. 1993 Aug 16;194(3):1090-6. doi: 10.1006/bbrc.1993.1933.

Abstract

A new mutation of transthyretin (TTR) has been identified in a patient with late-onset familial amyloidotic polyneuropathy (FAP) of Japanese origin. Peptide mapping by reverse-phase high performance liquid chromatography to compare the patient's TTR with normal TTR showed the presence of an abnormal peptide. Amino acid sequence analysis of the peptide (residues 49-61) showed a lysine-for-glutamic acid substitution at position 61. This substitution, verified by direct DNA sequencing, was the result of a guanine to adenine change on exon 3 of the TTR gene. A polymerase chain reaction-induced mutation restriction analysis (PCR-IMRA) system was established to rapidly detect the missense mutation. TTR-Lys61 is the first variant TTR with a replacement of the acidic with basic amino acid to be found in the amyloid precursor proteins of FAP.

Publication types

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

MeSH terms

  • Aged
  • Aged, 80 and over
  • Amino Acid Sequence
  • Asian People
  • Base Sequence
  • Exons / genetics
  • Female
  • Hereditary Sensory and Motor Neuropathy / genetics*
  • Humans
  • Japan
  • Male
  • Middle Aged
  • Molecular Sequence Data
  • Mutation / genetics*
  • Pedigree
  • Peptide Mapping
  • Polymerase Chain Reaction
  • Prealbumin / genetics*
  • Protein Precursors / genetics
  • Sequence Analysis
  • Sequence Homology, Amino Acid
  • Sequence Homology, Nucleic Acid

Substances

  • Prealbumin
  • Protein Precursors