Evidence map›Paper›PMID 23199516›Full record

ArticleJournal of the American College of Cardiology2013

Interferon-γ activates expression of p15 and p16 regardless of 9p21.3 coronary artery disease risk genotype.

Naif A M Almontashiri, Meng Fan, Brian L M Cheng, Hsiao-Huei Chen, Robert Roberts, Alexandre F R Stewart

Abstract read
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In one paragraph

Article in Journal of the American College of Cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Roles of the Chr.9p21.3Frontiers in cardiovascular medicine · 2018
    Article
  10. Review
  11. Article
  12. Molecular genetics of coronary artery disease.Journal of human genetics · 2016
    Review
  13. Genome-wide association studies of late-onset cardiovascular disease.Journal of molecular and cellular cardiology · 2015
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Genetics of coronary artery disease: an update.Methodist DeBakey cardiovascular journal
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Naif A M AlmontashiriDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada.
Meng Fan
Brian L M Cheng
Hsiao-Huei Chen
Robert Roberts
Alexandre F R Stewart
University of Ottawa · CAOttawa Hospital · CA

Funding

Canadian Institutes of Health Research MOP179197Canadian Institutes of Health Research MOP77682Canadian Institutes of Health Research MOP82810
6 · The paper itself

Abstract

objectivesBecause post-transcriptional mechanisms modulate levels of p16 (encoded by CDKN2A) and p15 (encoded by CDKN2B), we tested whether interferon-γ regulates the expression of these proteins and the effect of the 9p21 genotype.

backgroundThe mechanism whereby the common variant at chromosome 9p21.3 confers risk for coronary artery disease (CAD) remains uncertain. A recent report proposed that 9p21.3 confers differential activation of adjacent genes in response to interferon-γ, and reported that mRNA levels of CDKN2B are reduced in response to interferon-γ.

methodsHuman umbilical vein endothelial cells (HUVECs), aortic smooth muscle cells, HeLa cells, HEK293 cells, and 16 human lymphoblastoid cell lines, all genotyped for the 9p21.3 locus, were treated with interferon-γ and analyzed by immunoblot.

resultsIn all cells tested--except HUVECs where expression was not modulated by interferon-γ--regardless of 9p21.3 genotype, interferon-γ increased the expression of p16 and p15. Northern blot analysis confirmed that interferon-γ has little effect on mRNA levels of CDKN2A and CDKN2B.

conclusionsThe 9p21.3 risk genotype does not affect the activation of cyclin-dependent kinase inhibitors p15 and p16 by interferon-γ. Thus, another mechanism is likely to account for the CAD risk associated with this locus.

Indexed as

Blotting, NorthernCells, CulturedChromosomes, Human, Pair 9Coronary Artery DiseaseCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16DNA PrimersGene ExpressionGenotypeHEK293 CellsHeLa CellsHumansHuman Umbilical Vein Endothelial CellsImmunoblottingInterferon-gammaMuscle, Smooth, VascularCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16DNA PrimersInterferon-gammaRNA, Messenger

Identifiers

PMID23199516
OpenAlexW2033328647

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.