Evidence map›Paper›PMID 7883971›Full record

ArticleThe Journal of clinical investigation1995

Familial ligand-defective apolipoprotein B. Identification of a new mutation that decreases LDL receptor binding affinity.

C R Pullinger, L K Hennessy, J E Chatterton, W Liu, J A Love, C M Mendel, P H Frost, M J Malloy, V N Schumaker, J P Kane

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed.

  1. Review
  2. Article
  3. Journal of the American Heart Association · 2023
    Article
  4. Review
  5. Identification and Functional Analysis ofInternational journal of molecular sciences · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Genetics of familial hypercholesterolemia.Current atherosclerosis reports · 2015
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

C R PullingerCardiovascular Research Institute, University of California, San Francisco 94143.
L K Hennessy
J E Chatterton
W Liu
J A Love
C M Mendel
P H Frost
M J Malloy
V N Schumaker
J P Kane

Funding

Systems genomics of metabolic syndrome traitsP01HL028481 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI REUE, KAREN · 1985 to 2019
$50.2M
SYNTHESIS AND SECRETION OF NORMAL AND ABNORMAL LIPOPROTEINSP50HL014237 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI HAVEL, RICHARD J · 1985 to 1996
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LIPOPROTEIN LIPASE DEFICIENCY: GENETICS AND BIOCHEMISTRYR01HL045753 · NHLBI · UNIVERSITY OF UTAH · PI LALOUEL, JEAN-MARC · 1991 to 1995
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NHLBI NIH HHS HL-14237NHLBI NIH HHS HL-28481NHLBI NIH HHS HL-45753-02
6 · The paper itself

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.

Indexed as

Point MutationAdultAmino Acid SequenceApolipoproteins BArginineArteriosclerosisBase SequenceCholesterolFemaleGenetic MarkersHaplotypesHumansHypercholesterolemiaIndians, North AmericanMaleMolecular Sequence DataApolipoproteins BArginineCholesterolGenetic MarkersReceptors, LDL

Identifiers

PMID7883971
PMCPMC441461

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.