Evidence map›Paper›PMID 26011126›Full record

ArticlePloS one2015

A Function for the hnRNP A1/A2 Proteins in Transcription Elongation.

Bruno Lemieux, Marco Blanchette, Anne Monette, Andrew J Mouland, Raymund J Wellinger, Benoit Chabot

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 40 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Age and 17β-Estradiol (ENon-coding RNA · 2023
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  11. Review
  12. HNRNPA1-induced spliceopathy in a transgenic mouse model of myotonic dystrophy.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  13. Novel Non-Coding Transcript inFrontiers in oncology · 2020
    Article
  14. Cellular consequences of arginine methylation.Cellular and molecular life sciences : CMLS · 2019
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Linking hnRNP Function to ALS and FTD Pathology.Frontiers in neuroscience · 2018
    Review
  20. Review
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

6 authors at 4 institutions in 2 countries.

Bruno LemieuxRNA group and Department of Microbiology and Infectious Diseases, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Quebec, Canada.
Marco BlanchetteStowers Institute for Medical Research, Kansas City, Missouri, United States of America.
Anne MonetteLady Davis Institute for Medical Research-Sir Mortimer B. Davis Jewish General Hospital, McGill University, Montreal, Quebec, Canada.
Andrew J MoulandLady Davis Institute for Medical Research-Sir Mortimer B. Davis Jewish General Hospital, McGill University, Montreal, Quebec, Canada.
Raymund J WellingerRNA group and Department of Microbiology and Infectious Diseases, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Quebec, Canada.
Benoit ChabotRNA group and Department of Microbiology and Infectious Diseases, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Quebec, Canada.
Université de Sherbrooke · CAJewish General Hospital · CAMcGill University · CAStowers Institute for Medical Research · US

Funding

Canadian Institutes of Health Research MOP56794Canadian Institutes of Health Research MOP93917Canadian Institutes of Health Research MOP97874
6 · The paper itself

Abstract

The hnRNP A1 and A2 proteins regulate processes such as alternative pre-mRNA splicing and mRNA stability. Here, we report that a reduction in the levels of hnRNP A1 and A2 by RNA interference or their cytoplasmic retention by osmotic stress drastically increases the transcription of a reporter gene. Based on previous work, we propose that this effect may be linked to a decrease in the activity of the transcription elongation factor P-TEFb. Consistent with this hypothesis, the transcription of the reporter gene was stimulated when the catalytic component of P-TEFb, CDK9, was inhibited with DRB. While low levels of A1/A2 stimulated the association of RNA polymerase II with the reporter gene, they also increased the association of CDK9 with the repressor 7SK RNA, and compromised the recovery of promoter-distal transcription on the Kitlg gene after the release of pausing. Transcriptome analysis revealed that more than 50% of the genes whose expression was affected by the siRNA-mediated depletion of A1/A2 were also affected by DRB. RNA polymerase II-chromatin immunoprecipitation assays on DRB-treated and A1/A2-depleted cells identified a common set of repressed genes displaying increased occupancy of polymerases at promoter-proximal locations, consistent with pausing. Overall, our results suggest that lowering the levels of hnRNP A1/A2 elicits defective transcription elongation on a fraction of P-TEFb-dependent genes, hence favoring the transcription of P-TEFb-independent genes.

Indexed as

Transcription Elongation, GeneticAlternative SplicingCell LineCyclin-Dependent Kinase 9CytoplasmDichlororibofuranosylbenzimidazoleGenes, ReporterHCT116 CellsHeterogeneous Nuclear Ribonucleoprotein A1Heterogeneous-Nuclear Ribonucleoprotein Group A-BHumansModels, BiologicalOsmotic PressurePositive Transcriptional Elongation Factor BRNA InterferenceRNA Polymerase IICDK9 protein, humanCyclin-Dependent Kinase 9DichlororibofuranosylbenzimidazoleHeterogeneous Nuclear Ribonucleoprotein A1Heterogeneous-Nuclear Ribonucleoprotein Group A-BhnRNP A2Positive Transcriptional Elongation Factor BRNA Polymerase IIRNA, Small Interfering

Identifiers

PMID26011126
PMCPMC4444011
OpenAlexW353059511

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.