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Polymorphism and deficiency of human factor H-related proteins p39 and p37

E Feifel1, W M Prodinger, M Mölgg

  • 1Institut für Hygiene, Leopold-Franzens University, Innsbruck, Austria.

Immunogenetics
|January 1, 1992
PubMed

Insights

This study identifies genetic variations in factor H-related proteins (p39/p37) in human serum, revealing a common polymorphism with three distinct patterns. These variations follow autosomal Mendelian inheritance, impacting protein recognition by specific antibodies.

Area of Science:

  • Immunogenetics
  • Molecular Biology
  • Human Genetics

Background:

  • A novel factor H-related 1.4 kilobase mRNA codes for serum proteins p39/p37.
  • Recombinant proteins from cDNA clones show variations in epitope expression recognized by monoclonal antibody (mAb) 3D11.
  • These variations likely stem from differences in amino acid sequences.

Purpose of the Study:

  • To investigate corresponding alterations in native p39/p37 proteins in human sera.
  • To characterize the polymorphism of factor H-related proteins p39 and p37.
  • To determine the inheritance pattern of these protein variations.

Main Methods:

  • Western blot analysis of human sera using mAb 3D11 and a polyclonal factor H-specific antiserum.
  • Detection of three distinct protein patterns (FH1.4p+m+, FH1.4p+m-, FH1.4p-m-).
  • Family studies involving 98 individuals from 27 families and Southern blot analysis.

Main Results:

  • Three phenotypes were identified in the healthy population with frequencies of 0.556, 0.40, and 0.044.
  • Allele frequencies were estimated as FH1.4*p+m+ (0.33), FH1.4*p+m- (0.46), and FH1.4*p-m- (0.21) under Hardy-Weinberg equilibrium.
  • Autosomal Mendelian inheritance was confirmed through family studies, supporting a polymorphism in factor H-related proteins.

Conclusions:

  • A common polymorphism exists for factor H-related proteins p39 and p37 in human populations.
  • This polymorphism affects the recognition of these proteins by specific antibodies.
  • The inheritance pattern is autosomal Mendelian, providing insights into complement system regulation.

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