ArticleThe Journal of clinical investigation1995
Familial ligand-defective apolipoprotein B. Identification of a new mutation that decreases LDL receptor binding affinity.
Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
44 citing papers in PubMed.
- The Spectrum of Genetic Causes of Familial Hypercholesterolemia Phenotype.Current atherosclerosis reports · 2026Review
- Article
- Article
- Current Data and New Insights into the Genetic Factors of Atherogenic Dyslipidemia Associated with Metabolic Syndrome.Diagnostics (Basel, Switzerland) · 2023Review
- Identification and Functional Analysis ofInternational journal of molecular sciences · 2023Article
- Opportunistic Genetic Screening for Familial Hypercholesterolemia in Heart Transplant Patients.Journal of clinical medicine · 2023Article
- Clinical Evaluation of Patients with Genetically Confirmed Familial Hypercholesterolemia.Journal of clinical medicine · 2023Article
- Article
- Etiologic Puzzle of Coronary Artery Disease: How Important Is Genetic Component?Life (Basel, Switzerland) · 2022Review
- Whole-exome sequencing reveals damaging gene variants associated with hypoalphalipoproteinemia.Journal of lipid research · 2022Article
- Genetic Regulatory Networks of Apolipoproteins and Associated Medical Risks.Frontiers in cardiovascular medicine · 2021Review
- The Digenic Causality in Familial Hypercholesterolemia: Revising the Genotype-Phenotype Correlations of the Disease.Frontiers in genetics · 2020Review
- Three patients with homozygous familial hypercholesterolemia: Genomic sequencing and kindred analysis.Molecular genetics & genomic medicine · 2019Article
- PCSK9 inhibitor access barriers-issues and recommendations: Improving the access process for patients, clinicians and payers.Clinical cardiology · 2017Review
- A novel indel variant in LDLR responsible for familial hypercholesterolemia in a Chinese family.PloS one · 2017Article
- Exploring the complete mutational space of the LDL receptor LA5 domain using molecular dynamics: linking SNPs with disease phenotypes in familial hypercholesterolemia.Human molecular genetics · 2016Article
- Genetics of coronary artery disease and myocardial infarction.World journal of cardiology · 2016Review
- Structural analysis of APOB variants, p.(Arg3527Gln), p.(Arg1164Thr) and p.(Gln4494del), causing Familial Hypercholesterolaemia provides novel insights into variant pathogenicity.Scientific reports · 2015Article
- Genetics of familial hypercholesterolemia.Current atherosclerosis reports · 2015Review
- Impact of 3'UTR genetic variants in PCSK9 and LDLR genes on plasma lipid traits and response to atorvastatin in Brazilian subjects: a pilot study.International journal of clinical and experimental medicine · 2015Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Detection of new ligand-defective mutations of apolipoprotein B (apoB) will enable identification of sequences involved in binding to the LDL receptor. Genomic DNA from patients attending a lipid clinic was screened by single-strand conformation polymorphism analysis for novel mutations in the putative LDL receptor-binding domain of apoB-100. A 46-yr-old woman of Celtic and Native American ancestry with primary hypercholesterolemia (total cholesterol [TC] 343 mg/dl; LDL cholesterol [LDL-C] 241 mg/dl) and pronounced peripheral vascular disease was found to be heterozygous for a novel Arg3531-->Cys mutation, caused by a C-->T transition at nucleotide 10800. One unrelated 59-yr-old man of Italian ancestry was found with the same mutation after screening 1,560 individuals. He had coronary heart disease, a TC of 310 mg/dl, and an LDL-C of 212 mg/dl. A total of eight individuals were found with the defect in the families of the two patients. They had an age- and sex-adjusted TC of 240 +/- 14 mg/dl and LDL-C of 169 +/- 10 mg/dl. This compares with eight unaffected family members with age- and sex-adjusted TC of 185 +/- 12 mg/dl and LDL-C of 124 +/- 12 mg/dl. In a dual-label fibroblast binding assay, LDL from the eight subjects with the mutation had an affinity for the LDL receptor that was 63% that of control LDL. LDL from eight unaffected family members had an affinity of 91%. By way of comparison, LDL from six patients heterozygous for the Arg3500-->Gln mutation had an affinity of 36%. The percentage mass ratio of the defective Cys3531 LDL to normal LDL was 59:41, as determined using the mAb MB19 and dynamic laser light scattering. Thus, the defective LDL had accumulated in the plasma of these patients. Using this mass ratio, it was calculated that the defective Cys3531 LDL particles bound with 27% of normal affinity. Deduced haplotypes using 10 apoB gene markers showed the Arg3531-->Cys alleles to be different in the two kindreds and indicates that the mutations arose independently. The Arg3531-->Cys mutation is the second reported cause of familial ligand-defective apoB.
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