Abstract
Family, twin and population studies have uncovered significant effects of genes on levels of risk factors or protective factors with respect to coronary heart disease (CHD)1,2 and it is an important task to uncover the individual genes contributing to risk-factor heritability. Current attempts to identify such genes follow the ‘candidate gene’ approach1–5. Among the candidate genes with respect to coronary heart disease (CHD), the apolipoprotein genes have been the focus of much research. Candidate gene studies conducted at the level of LDL allotypes or apolipoprotein E isoforms before DNA technology became available uncovered effects of normal genes at the apolipoprotein B (apoB) and apolipoprotein E (apoE) loci on lipid levels. With the advent of DNA technology, the potential for studies employing the candidate gene approach was dramatically expanded and numerous studies on restriction fragment length polymorphisms (RFLPs) at apolipoprotein loci and risk factor levels or overt disease have been reported.
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© 1994 Springer Science+Business Media Dordrecht
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Pedersen, J.C., Berg, K. (1994). Normal Polymorphism at the Low Density Lipoprotein Receptor (LDLR) Locus: Effect on Cholesterol Levels and Interaction with Apolipoprotein E (apoE) Genes. In: Goldbourt, U., de Faire, U., Berg, K. (eds) Genetic factors in coronary heart disease. Developments in Cardiovascular Medicine, vol 156. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-1130-0_22
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DOI: https://doi.org/10.1007/978-94-011-1130-0_22
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