Evidence map›Paper›PMID 24396277›Full record

ArticleCurrent genomics2013

Genetics of the first seven proprotein convertase enzymes in health and disease.

Hannu Turpeinen, Zsuzsanna Ortutay, Marko Pesu

Open access · bronzeAbstract read
In one paragraph

Article in Current genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
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  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. A novel mutation in the mouse Pcsk1 gene showing obesity and diabetes.Mammalian genome : official journal of the International Mammalian Genome Society · 2020
    Article
  13. Article
  14. Article
  15. Functional analysis of corin protein domains required for PCSK6-mediated activation.The international journal of biochemistry & cell biology · 2018
    Article
  16. Review
  17. PCSK9 inhibitors in the prevention of cardiovascular disease.Journal of thrombosis and thrombolysis · 2016
    Review
  18. PCSK1 Variants and Human Obesity.Progress in molecular biology and translational science · 2016
    Review
  19. Association ofBiomedical reports · 2015
    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

3 authors at 1 institution in 1 country.

Hannu TurpeinenImmunoregulation, Institute of Biomedical Technology, University of Tampere, and BioMediTech, Tampere, Finland;
Zsuzsanna OrtutayImmunoregulation, Institute of Biomedical Technology, University of Tampere, and BioMediTech, Tampere, Finland;
Marko PesuImmunoregulation, Institute of Biomedical Technology, University of Tampere, and BioMediTech, Tampere, Finland; ; Fimlab laboratories, Pirkanmaa Hospital District, Finland.
Tampere University · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Members of the substilisin/kexin like proprotein convertase (PCSK) protease family cleave and convert immature pro-proteins into their biologically active forms. By cleaving for example prohormones, cytokines and cell membrane proteins, PCSKs participate in maintaining the homeostasis in a healthy human body. Conversely, erratic enzymatic function is thought to contribute to the pathogenesis of a wide variety of diseases, including obesity and hypercholestrolemia. The first characterized seven PCSK enzymes (PCSK1-2, FURIN, PCSK4-7) process their substrates at a motif made up of paired basic amino acid residues. This feature results in a variable degree of biochemical redundancy in vitro, and consequently, shared substrate molecules between the different PCSK enzymes. This redundancy has confounded our understanding of the specific biological functions of PCSKs. The physiological roles of these enzymes have been best illustrated by the phenotypes of genetically engineered mice and patients that carry mutations in the PCSK genes. Recent developments in genome-wide methodology have generated a large amount of novel information on the genetics of the first seven proprotein convertases. In this review we summarize the reported genetic alterations and their associated phenotypes.

Indexed as

Association.FURINGeneticsProprotein convertase

Identifiers

PMID24396277
PMCPMC3867721
OpenAlexW2029863970

What OpenQuestion holds

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LicenceCC BY-NC
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.