Transferrin receptor mutation analysis in hereditary hemochromatosis patients

Blood Cells Mol Dis. 1998 Sep;24(3):317-21. doi: 10.1006/bcmd.1998.0199.

Abstract

The Cys282-->Tyr mutation in the HFE gene is carried by the majority of hereditary hemochromatosis patient chromosomes, yet some patients do not seem to harbor any mutation in this gene. This suggests a possibility that these patients may have a mutation in other genes in the same pathway as HFE. We analyzed the cDNA sequences of transferrin receptor (TFR), which was recently shown to interact with HFE, in twenty-one hereditary hemochromatosis patients including sixteen individuals who did not carry a Cys282-->Tyr mutation. A nucleotide substitution (424A-->G), which resulted in the Ser142-->Gly amino acid substitution, was the only amino acid polymorphism detected in the open reading frame of the TFR gene in these patients. This amino acid substitution was a rather common polymorphism in the general population (49%) and its frequency did not significantly differ in the hereditary hemochromatosis (HH) patients regardless of the HFE genotype. Thus, amino acid changes in the TFR gene do not appear to play a role in HH even when the patients do not have a HFE mutation. However, this study does not rule out the possibility of the involvement of mutations in non-coding regions.

MeSH terms

  • Amino Acid Substitution
  • DNA, Complementary / genetics
  • Genetic Heterogeneity
  • Genetic Predisposition to Disease
  • Genotype
  • HLA Antigens / genetics
  • Hemochromatosis / genetics*
  • Hemochromatosis Protein
  • Histocompatibility Antigens Class I / genetics
  • Humans
  • Membrane Proteins*
  • Mutation*
  • Mutation, Missense
  • Open Reading Frames
  • Point Mutation
  • Polymorphism, Genetic
  • Receptors, Transferrin / genetics*
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • DNA, Complementary
  • HFE protein, human
  • HLA Antigens
  • Hemochromatosis Protein
  • Histocompatibility Antigens Class I
  • Membrane Proteins
  • Receptors, Transferrin