The genetics of the Lp Antigen

Sing, Charles F.; Schultz, Jerome S.; Shreffler, Donald C.

doi:10.1111/j.1469-1809.1974.tb01992.x

Cited by 75 publications

(10 citation statements)

References 17 publications

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“…The concordance of Lp(a) levels among siblings with the apo(a) genotype suggest that factors at the apo(a) locus than number ofkringle 4 repeats are contributing to the pl; Lp(a) level. (27,28 After the original suggestion of Utermann and co-workers (12), several investigators have noted an inverse relationship between the size of the apo(a) protein and the amount of plasma Lp(a) (13,16,30 (22,(50)(51)(52)(53). A problem which has been encountered when the apo(a) protein have been used for segregation analysis, is that the isoforms are not in Hardy-Weinberg equilibrium (12)(13)(14)(15)(16).…”

Section: Resultsmentioning

confidence: 99%

Molecular basis of apolipoprotein (a) isoform size heterogeneity as revealed by pulsed-field gel electrophoresis.

Lackner¹,

Boerwinkle²,

Leffert³

et al. 1991

J. Clin. Invest.

392

206

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Lipoprotein (a) [Lp(a)J is a cholesterol-rich lipoprotein that is distinguished by its content ofa glycoprotein called apolipoprotein(a) Iapo(a)I. Apo(a) varies in size among individuals owing to different numbers ofcysteine-rich sequences that are homologous to kringle 4 of plasminogen. The genetic basis for this variation is not understood at the genomic level. In this study we used pulsed-field gel electrophoresis and genomic blotting to identify a highly polymorphic restriction fragment from the apo(a) gene. The fragment contains multiple tandem repeats of a kringle 4-encoding sequence and varies in length from 48 to 190 kb depending on the number of kringle 4-encoding sequences. A total of 19 different alleles were identified among 102 unrelated Caucasian Americans. 94% of individuals studied had two different alleles which could be distinguished by size on pulsed-field gel electrophoresis. The degree of size heterogeneity was much greater than had been previously appreciated based on the analysis of the apparent molecular mass of the protein.The size of the apo(a) gene correlated directly with the size of the apo(a) protein, and inversely with the concentration of Lp(a) in plasma. Segregation analysis of the apo(a) gene was performed in families; siblings with identical apo(a) genotypes had similar plasma levels of Lp(a). These results suggest that in the normal population, the level of plasma Lp(a) is largely determined by alleles at the apo(a) locus. (J. Clin.

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Section: Resultsmentioning

confidence: 99%

Molecular basis of apolipoprotein (a) isoform size heterogeneity as revealed by pulsed-field gel electrophoresis.

Lackner¹,

Boerwinkle²,

Leffert³

et al. 1991

J. Clin. Invest.

392

206

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“…The Lp(a) lipoprotein exhibits a quantitative genetic polymorphism (28,29) and the Lp(a) specific glycoprotein (apo (a)) shows a qualitative genetic polymorphism (21). 14 of the 18 patients showed significant changes (defined as at least twofold) in Lp(a) lipoprotein plasma concentration (Table III).…”

Section: Resultsmentioning

confidence: 99%

Changes of genetic apolipoprotein phenotypes caused by liver transplantation. Implications for apolipoprotein synthesis.

Kraft¹,

Menzel²,

Hoppichler³

et al. 1989

J. Clin. Invest.

236

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Liver transplantation provides a unique opportunity to investigate the contribution in vivo of the liver to the synthesis and degradation of genetically polymorphic plasma proteins. We have determined the genetic polymorphisms of apo A-IV, apo E, and of the Lp(a) glycoprotein (apo (a)) in the plasma of subjects undergoing liver transplantation and in respective organ donors. The results show that in humans, > 90% of the plasma apo E and virtually all apo (a) are liver derived, whereas this organ does not significantly contribute to plasma apo A-IV levels.

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“…>30 mg/dl is considered to be genetically or racially determined [6], the level is often found to be higher in patients with IDDM than in healthy control subjects as reported by Rudberg and Persson [7]. They concluded that Lp(a) was elevated during puberty in normoalbuminuric subjects with IDDM, independent of metabolic control and IGF-I.…”

Section: Introductionmentioning

confidence: 90%

Association of Angiotensin-Converting Enzyme Gene Polymorphism with Lipid Profiles in Children and Adolescents with Insulin-Dependent Diabetes mellitus

Kobayashi¹,

Amemiya²,

Mochizuki³

et al. 1999

Horm Res Paediatr

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We attempted to clarify the association between angiotensin-converting enzyme (ACE) gene polymorphism and the other predictive factors for macroangiopathy in children and adolescents with uncomplicated insulin-dependent diabetes mellitus (IDDM). Sixty-three patients were divided into 3 groups according to the ACE genotypes. The lipid profiles were evaluated according to ACE genotypes. The level of lipoprotein(a) (Lp(a)) in the II genotype was significantly lower than that in groups with the D allele. Lp(a) significantly correlated with apo B/apo A-I (p < 0.001, r = 0.63) and atherogenic index (AI = (total cholesterol – high-density lipoprotein cholesterol)/high-density lipoprotein cholesterol; p = 0.004, r = 0.36). We suggest that the D allele may affect the level of Lp(a) and the other lipid profiles in IDDM.

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The genetics of the Lp Antigen

Cited by 75 publications

References 17 publications

Molecular basis of apolipoprotein (a) isoform size heterogeneity as revealed by pulsed-field gel electrophoresis.

Molecular basis of apolipoprotein (a) isoform size heterogeneity as revealed by pulsed-field gel electrophoresis.

Changes of genetic apolipoprotein phenotypes caused by liver transplantation. Implications for apolipoprotein synthesis.

Association of Angiotensin-Converting Enzyme Gene Polymorphism with Lipid Profiles in Children and Adolescents with Insulin-Dependent Diabetes mellitus

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