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Polymerization defect of fibrinogen Baltimore III due to a gamma Asn308----Ile mutation

S Bantia1, W R Bell, C V Dang

  • 1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.

Blood
|April 15, 1990
PubMed

Insights

Fibrinogen Baltimore III, a variant fibrinogen, has a mutation in its gamma-chain (Asn308 to Ile). This alteration impairs fibrin polymerization, highlighting the critical role of gamma Asn308 in clot formation.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Hematology

Background:

  • Congenital dysfibrinogenemia involves abnormal fibrinogen function.
  • Fibrinogen Baltimore III exhibits impaired fibrin monomer polymerization.
  • The gamma-chain variant shows altered molecular weight on SDS-PAGE.

Purpose of the Study:

  • To identify the molecular defect in Fibrinogen Baltimore III.
  • To investigate the role of gamma-chain residue 308 in fibrin polymerization.

Main Methods:

  • Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE).
  • Reverse phase high-performance liquid chromatography (HPLC) of lysyl endopeptidase digests.
  • Amino acid sequence analysis.
  • Concanavalin A binding assays.

Main Results:

  • Identified a unique peptide in the digest of Fibrinogen Baltimore III gamma-chain.
  • Determined the mutation: Asn308 replaced by isoleucine (Asn308Ile).
  • Confirmed carbohydrate moiety is unaltered and not responsible for electrophoretic mobility changes.

Conclusions:

  • The integrity of gamma Asn308 is crucial for normal fibrin monomer polymerization.
  • Alterations at residue 308 (e.g., to Lys or Ile) significantly delay fibrinogen to fibrin conversion.

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