Evidence map›Paper›PMID 1336760›Full record

ArticleHuman genetics1992

The apolipoprotein (a) gene: a transcribed hypervariable locus controlling plasma lipoprotein (a) concentration.

H G Kraft, S Köchl, H J Menzel, C Sandholzer, G Utermann

Abstract read
PubMed Publisher
In one paragraph

Article in Human genetics, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 3 pooled it
17.1field-weighted citation impact, top 1% of its field
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

57 citing papers in PubMed, 3 syntheses or guidelines pooled it, 272 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Review
  7. Article
  8. Article
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  10. Article
  11. Review
  12. Lipoprotein(a): from Causality to Treatment.Current atherosclerosis reports · 2024
    Review
  13. Review
  14. Lipoprotein(a): a Case for Universal Screening in Youth.Current atherosclerosis reports · 2023
    Review
  15. Article
  16. Article
  17. Review
  18. Lipoprotein(a).Handbook of experimental pharmacology · 2022
    Article
  19. Article
  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

5 authors at 1 institution in 1 country.

H G KraftInstitut für Medizinische Biologie und Humangenetik, Universität Innsbruck, Austria.
S Köchl
H J Menzel
C Sandholzer
G Utermann
Universität Innsbruck · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipoprotein(a) [Lp(a)] is a quantitative trait in human plasma. Lp(a) consists of a low-density lipoprotein and the plasminogen-related apolipoprotein(a) [apo(a)]. The apo(a) gene determines a size polymorphism of the protein, which is related to Lp(a) levels in plasma. In an attempt to gain a deeper insight into the genetic architecture of this risk factor for coronary heart disease, we have investigated the basis of the apo(a) size polymorphism by pulsed field gel electrophoresis of genomic DNA employing various restriction enzymes (SwaI, KpnI, KspI, SfiI, NotI) and an apo(a) kringle-IV-specific probe. All enzymes detected the same size polymorphism in the kringle IV repeat domain of apo(a). With KpnI, 26 different alleles were identified among 156 unrelated subjects; these alleles ranged in size from 32 kb to 189 kb and differed by increments of 5.6 kb, corresponding to one kringle IV unit. There was a perfect match between the size of the apo(a) DNA phenotypes and the size of apo(a) isoforms in plasma. The apo(a) DNA polymorphism was further used to estimate the magnitude of the apo(a) gene effect on Lp(a) levels by a sib-pair comparison approach based on 253 sib-pairs from 64 families. Intra-class correlation of log-transformed Lp(a) levels was high in sib-pairs sharing both parental alleles (r = 0.91), significant in those with one common allele (r = 0.31), and absent in those with no parental allele in common (r = 0.12). The data show that the intra-individual variability in Lp(a) levels is almost entirely explained by variation at the apo(a) locus but that only a fraction (46%) is explained by the DNA size polymorphism. This suggests further heterogeneity relating to Lp(a) levels in the apo(a) gene.

Indexed as

AllelesApolipoproteins ABase SequenceChromosome MappingDeoxyribonucleases, Type II Site-SpecificDNAElectrophoresis, Gel, Pulsed-FieldExonsGene FrequencyHumansIntronsLipoprotein(a)Molecular Sequence DataPeptide FragmentsPolymerase Chain ReactionPolymorphism, GeneticApolipoproteins ADeoxyribonucleases, Type II Site-SpecificDNAGGTACC-specific type II deoxyribonucleasesLipoprotein(a)Peptide Fragments

Identifiers

PMID1336760
OpenAlexW2053361508

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.