Literature DB >> 2434069

Apolipoprotein B allotypes MB19(1) and MB19(2) in subjects with coronary artery disease and hypercholesterolemia.

S G Young, S J Bertics, T M Scott, B W Dubois, W F Beltz, L K Curtiss, J L Witztum.   

Abstract

We recently characterized a common form of genetic polymorphism in human apolipoprotein (apo) B, using the specific monoclonal antibody MB19 (Young SG, et al. Proc Natl Acad Sci USA 1986; 83:1101-1105). Antibody MB19 binds apo B with one of three distinct patterns of immunoreactivity (strong, intermediate, or weak). These three binding patterns are the result of the codominant inheritance of two common apo B alleles which encode for apo B allotypes MB19(1) and MB19(2), which have high and low affinity, respectively, for antibody MB19. Thus, subjects with strong or weak binding patterns are homozygous for MB19(1) or MB19(2), respectively, whereas those with an intermediate pattern are heterozygotes. To assess whether the MB19 polymorphism was related to hypercholesterolemia (HC) or to coronary artery disease (CAD), we determined the MB19 binding pattern and plasma lipoprotein concentrations in 129 normal subjects, 51 patients with HC, and 149 patients with CAD. The percentages of normal subjects having the strong, intermediate, and weak binding patterns were 11.6%, 41.9%, and 46.5%, respectively. The frequency of the three MB19 binding patterns was nearly the same in the groups with HC and CAD. Also, within each of the three groups of subjects, the MB19 binding pattern did not influence the plasma lipoprotein concentrations. We conclude that the genetic polymorphism in apo B defined by antibody MB19 is a common allelic variation in apo B, and that in the populations studied, it does not appear to be associated with the development of coronary artery disease or hypercholesterolemia.

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Year:  1987        PMID: 2434069     DOI: 10.1161/01.atv.7.1.61

Source DB:  PubMed          Journal:  Arteriosclerosis        ISSN: 0276-5047


  5 in total

1.  A multilocus genotyping assay for candidate markers of cardiovascular disease risk.

Authors:  S Cheng; M A Grow; C Pallaud; W Klitz; H A Erlich; S Visvikis; J J Chen; C R Pullinger; M J Malloy; G Siest; J P Kane
Journal:  Genome Res       Date:  1999-10       Impact factor: 9.043

2.  Phenotypes of apolipoprotein B and apolipoprotein E after liver transplantation.

Authors:  M F Linton; R Gish; S T Hubl; E Bütler; C Esquivel; W I Bry; J K Boyles; M R Wardell; S G Young
Journal:  J Clin Invest       Date:  1991-07       Impact factor: 14.808

3.  Genetic analysis of a kindred with familial hypobetalipoproteinemia. Evidence for two separate gene defects: one associated with an abnormal apolipoprotein B species, apolipoprotein B-37; and a second associated with low plasma concentrations of apolipoprotein B-100.

Authors:  S G Young; S J Bertics; L K Curtiss; B W Dubois; J L Witztum
Journal:  J Clin Invest       Date:  1987-06       Impact factor: 14.808

4.  Association of apolipoprotein B gene variants with plasma apoB and low density lipoprotein (LDL) cholesterol levels.

Authors:  S S Deeb; R A Failor; B G Brown; J D Brunzell; J J Albers; A G Motulsky; E Wijsman
Journal:  Hum Genet       Date:  1992-02       Impact factor: 4.132

5.  Apolipoprotein B polymorphism and altered apolipoprotein B and low density lipoprotein cholesterol concentrations in Finnish children.

Authors:  M J Tikkanen; J Viikari; H K Akerblom; E Pesonen
Journal:  Br Med J (Clin Res Ed)       Date:  1988-01-16
  5 in total

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