Evidence map›Paper›PMID 25208576›Full record

ArticleNature communications2014

Human Tra2 proteins jointly control a CHEK1 splicing switch among alternative and constitutive target exons.

Andrew Best, Katherine James, Caroline Dalgliesh, Elaine Hong, Mahsa Kheirolahi-Kouhestani, Tomaz Curk, Yaobo Xu, Marina Danilenko, Rafiq Hussain, Bernard Keavney and 10 more

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

42 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Ultra-Conserved Poison Exons Enable Rapid and Safe Splicing Factor Gene Expression Switches: A Hypothesis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Autoregulated splicing ofScience (New York, N.Y.) · 2024
    Article
  15. Article
  16. Review
  17. Review
  18. 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

20 authors at 4 institutions in 3 countries.

Andrew BestInstitute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle NE1 3BZ, UK.
Katherine JamesSchool of Computing Science, Claremont Tower, Newcastle University, Newcastle upon Tyne NE1 7RU, UK.
Caroline DalglieshInstitute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle NE1 3BZ, UK.
Elaine HongInstitute for Cellular Medicine, Newcastle University, Framlington Place, Newcastle NE2 4HH, UK.
Mahsa Kheirolahi-KouhestaniInstitute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle NE1 3BZ, UK.
Tomaz CurkFaculty of Computer and Information Science, University of Ljubljana, Trzaska cesta 25, SI-1000, Ljubljana, Slovenia.
Yaobo XuInstitute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle NE1 3BZ, UK.
Marina DanilenkoInstitute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle NE1 3BZ, UK.
Rafiq HussainInstitute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle NE1 3BZ, UK.
Bernard Keavney1] Institute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle NE1 3BZ, UK [2] Institute of Cardiovascular Sciences, The University of Manchester, Manchester M13 9NT, UK.
Anil WipatSchool of Computing Science, Claremont Tower, Newcastle University, Newcastle upon Tyne NE1 7RU, UK.
Roscoe KlinckDepartment of Microbiology and Infectious Diseases, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Québec, Canada J1E 4K8.
Ian G CowellInstitute for Cell and Molecular Biosciences, Newcastle University, Newcastle NE2 4HH, UK.
Ka Cheong LeeInstitute for Cell and Molecular Biosciences, Newcastle University, Newcastle NE2 4HH, UK.
Caroline A AustinInstitute for Cell and Molecular Biosciences, Newcastle University, Newcastle NE2 4HH, UK.
Julian P VenablesInstitute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle NE1 3BZ, UK.
Benoit ChabotDepartment of Microbiology and Infectious Diseases, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Québec, Canada J1E 4K8.
Mauro Santibanez KorefInstitute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle NE1 3BZ, UK.
Alison Tyson-CapperInstitute for Cellular Medicine, Newcastle University, Framlington Place, Newcastle NE2 4HH, UK.
David J ElliottInstitute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle NE1 3BZ, UK.
Newcastle University · GBUniversité de Sherbrooke · CAUniversity of Ljubljana · SIUniversity of Manchester · GB

Funding

Biotechnology and Biological Sciences Research Council BB/D013917/1Biotechnology and Biological Sciences Research Council BB/I006923/1Breast Cancer Now 2009NOVPHD21British Heart Foundation FS/10/008/28146British Heart Foundation FS/11/63/28944CIHR MOP93917Wellcome TrustWellcome Trust WT080368MAWellcome Trust WT089225/Z/09/Z
6 · The paper itself

Abstract

Alternative splicing--the production of multiple messenger RNA isoforms from a single gene--is regulated in part by RNA binding proteins. While the RBPs transformer2 alpha (Tra2α) and Tra2β have both been implicated in the regulation of alternative splicing, their relative contributions to this process are not well understood. Here we find simultaneous--but not individual--depletion of Tra2α and Tra2β induces substantial shifts in splicing of endogenous Tra2β target exons, and that both constitutive and alternative target exons are under dual Tra2α-Tra2β control. Target exons are enriched in genes associated with chromosome biology including CHEK1, which encodes a key DNA damage response protein. Dual Tra2 protein depletion reduces expression of full-length CHK1 protein, results in the accumulation of the DNA damage marker γH2AX and decreased cell viability. We conclude Tra2 proteins jointly control constitutive and alternative splicing patterns via paralog compensation to control pathways essential to the maintenance of cell viability.

Indexed as

Alternative SplicingExonsCell Line, TumorCheckpoint Kinase 1HumansMCF-7 CellsNerve Tissue ProteinsProtein KinasesRNA-Binding ProteinsRNA, MessengerSerine-Arginine Splicing FactorsCheckpoint Kinase 1CHEK1 protein, humanNerve Tissue ProteinsProtein KinasesRNA-Binding ProteinsRNA, MessengerSerine-Arginine Splicing FactorsTRA2A protein, humanTRA2B protein, human

Identifiers

PMID25208576
PMCPMC4175592
OpenAlexW2146487747

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.