Evidence map›Paper›PMID 27851963›Full record

ArticleCell reports2016

SRSF10 Connects DNA Damage to the Alternative Splicing of Transcripts Encoding Apoptosis, Cell-Cycle Control, and DNA Repair Factors.

Lulzim Shkreta, Johanne Toutant, Mathieu Durand, James L Manley, Benoit Chabot

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.0field-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

49 citing papers in PubMed, 96 citations in OpenAlex.

  1. Review
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  11. SRSF10 stabilizes CDC25A by triggering exon 6 skipping to promote hepatocarcinogenesis.Journal of experimental & clinical cancer research : CR · 2022
    Article
  12. Article
  13. Review
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  16. Exploring the multifunctionality of SR proteins.Biochemical Society transactions · 2022
    Article
  17. Article
  18. Review
  19. Article
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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 2 institutions in 2 countries.

Lulzim ShkretaDépartement de Microbiologie et d'Infectiologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, QC J1E 4K8, Canada.
Johanne ToutantDépartement de Microbiologie et d'Infectiologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, QC J1E 4K8, Canada.
Mathieu DurandLaboratory of Functional Genomics, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, QC J1E 4K8, Canada.
James L ManleyDepartment of Biological Sciences, Columbia University, New York, NY, 10027, USA.
Benoit ChabotDépartement de Microbiologie et d'Infectiologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, QC J1E 4K8, Canada. Electronic address: benoit.chabot@usherbrooke.ca.
Université de Sherbrooke · CAColumbia University · US

Funding

Regulation of RNA processing: Mechanisms and ConsequencesR35GM118136 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI James L. Manley · 2016 to 2026
$8.9M
MECHANISMS OF ALTERNATIVE SPLICING OF PRE MRNAR01GM048259 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI MANLEY, JAMES L. · 1992 to 2015
$5.2M
CIHR MOP-136948CIHR MOP-93917NIGMS NIH HHS R01 GM048259NIGMS NIH HHS R35 GM118136
6 · The paper itself

Abstract

RNA binding proteins and signaling components control the production of pro-death and pro-survival splice variants of Bcl-x. DNA damage promoted by oxaliplatin increases the level of pro-apoptotic Bcl-xS in an ATM/CHK2-dependent manner, but how this shift is enforced is not known. Here, we show that in normally growing cells, when the 5' splice site of Bcl-xS is largely repressed, SRSF10 partially relieves repression and interacts with repressor hnRNP K and stimulatory hnRNP F/H proteins. Oxaliplatin abrogates the interaction of SRSF10 with hnRNP F/H and decreases the association of SRSF10 and hnRNP K with the Bcl-x pre-mRNA. Dephosphorylation of SRSF10 is linked with these changes. A broader analysis reveals that DNA damage co-opts SRSF10 to control splicing decisions in transcripts encoding components involved in DNA repair, cell-cycle control, and apoptosis. DNA damage therefore alters the interactions between splicing regulators to elicit a splicing response that determines cell fate.

Indexed as

Alternative SplicingApoptosisbcl-X ProteinCell Cycle CheckpointsCell Cycle ProteinsCell LineDNA DamageDNA RepairHeterogeneous-Nuclear RibonucleoproteinsHumansModels, BiologicalOrganoplatinum CompoundsOxaliplatinPhosphorylationProtein BindingRepressor Proteinsbcl-X ProteinCell Cycle ProteinsHeterogeneous-Nuclear RibonucleoproteinsOrganoplatinum CompoundsOxaliplatinRepressor ProteinsRNA, MessengerRNA PrecursorsSerine-Arginine Splicing FactorsSRSF10 protein, humanalternative splicingapoptosiscell cyclecell fateDNA damage responseDNA repairhnRNP proteinsoxaliplatinphosphorylationRNA binding proteinssplicingSR proteins

Identifiers

PMID27851963
PMCPMC5483951
OpenAlexW2551428756

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.