ArticleProceedings of the National Academy of Sciences of the United States of America1989
Defects in the low density lipoprotein receptor gene affect lipoprotein (a) levels: multiplicative interaction of two gene loci associated with premature atherosclerosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Hormonal regulation of serum Lp (a) levels. Opposite effects after estrogen treatment and orchidectomy in males with prostatic carcinoma.The Journal of clinical investigation · 1992Trial
- Lipoprotein(a) in Familial Hypercholesterolemia.CJC open · 2024Article
- Lipoprotein(a) Genotype Influences the Clinical Diagnosis of Familial Hypercholesterolemia.Journal of the American Heart Association · 2023Article
- Lipoprotein(a) levels in children with suspected familial hypercholesterolaemia: a cross-sectional study.European heart journal · 2023Article
- Familial Hypercholesterolemia and Lipoprotein(a): A Gordian Knot in Cardiovascular Prevention.Metabolites · 2022Review
- Familial Hypercholesterolemia and Lipoprotein(a): Two Partners in Crime?Current atherosclerosis reports · 2022Review
- Improving Familial Hypercholesterolemia Diagnosis Using an EMR-based Hybrid Diagnostic Model.The Journal of clinical endocrinology and metabolism · 2022Article
- Lipoprotein(a).Handbook of experimental pharmacology · 2022Article
- Lipids and Lipoproteins in Health and Disease: Focus on Targeting Atherosclerosis.Biomedicines · 2021Review
- Lipoprotein (a): Recent Updates on a Unique Lipoprotein.Current atherosclerosis reports · 2021Review
- Structure, function, and genetics of lipoprotein (a).Journal of lipid research · 2016Review
- Transgenic rabbit models for studying human cardiovascular diseases.Comparative medicine · 2012Review
- Therapeutic potential of mipomersen in the management of familial hypercholesterolaemia.Drugs · 2012Article
- Lipoprotein (a) and other Lipid Profile in Patients with Thrombotic Stroke: Is it a Reliable Marker?Journal of laboratory physicians · 2011Article
- The interaction between coagulation factor 2 receptor and interleukin 6 haplotypes increases the risk of myocardial infarction in men.PloS one · 2010Article
- Hyperlipoproteinaemia(a) is a common cause of autosomal dominant hypercholesterolaemia.Journal of inherited metabolic disease · 2007Article
- Lipoprotein(a): biology and clinical importance.The Clinical biochemist. Reviews · 2004Article
- Sib-pair analysis detects elevated Lp(a) levels and large variation of Lp(a) concentration in subjects with familial defective ApoB.The Journal of clinical investigation · 1997Article
- The low density lipoprotein receptor is not required for normal catabolism of Lp(a) in humans.The Journal of clinical investigation · 1995Article
- Apolipoprotein(a) phenotypes and lipoprotein(a) concentrations in patients with hyperthyroidism.Journal of molecular medicine (Berlin, Germany) · 1995Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lipoprotein (a) [Lp(a)] contains two nonidentical protein species, apolipoprotein (apo) B-100 and a specific high molecular weight glycoprotein, apo(a). Lp(a) represents a continuous quantitative genetic trait, the genetics of which are only poorly understood. Genetic variation at the apo(a) locus affects plasma Lp(a) levels and explains at least 40% of the variability of this trait. Lp(a) levels were found to be elevated 3-fold in the plasma from patients with the heterozygous form of familial hypercholesterolemia who have one mutant low density lipoprotein receptor gene. This elevation was not due to a higher frequency of those apo(a) types that are associated with high Lp(a) levels in familial hypercholesterolemia patients. Rather Lp(a) levels were elevated for each of the apo(a) phenotypes examined. The effects of the apo(a) and low density lipoprotein receptor genes on Lp(a) levels are not additive but multiplicative. This is a situation not commonly considered in quantitative human genetics. We conclude that Lp(a) levels in plasma may be determined by variation at more than one gene locus.
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