Evidence map›Paper›PMID 25561496›Full record

ArticleGenes & development2015

Detained introns are a novel, widespread class of post-transcriptionally spliced introns.

Paul L Boutz, Arjun Bhutkar, Phillip A Sharp

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 281 papers.

0numbers the graph read from it
0cells of the map it votes in
281citing papers in PubMed
–field-weighted citation impact
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

281 citing papers in PubMed, 453 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Intron Retention Controls Localization of lncRNAsbioRxiv : the preprint server for biology · 2026
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Prevention of ubiquitination at K6 and K9 in mutant huntingtin exacerbates disease pathology in a knock-in mouse model.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  17. Article
  18. Review
  19. Review
  20. Article

221 more citing papers are in PubMed but not listed here.

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.

Paul L BoutzThe David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
Arjun BhutkarThe David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
Phillip A SharpThe David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA sharppa@mit.edu.
Massachusetts Institute of Technology · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
USE OF RETROVIRUS PROMOTER TRAP VECTORS TO IDENTIFY ONCOGENES AND ANTI-ONCOGENESP01CA042063 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI JACKS, TYLER E. · 1986 to 2021
$30.5M
REGULATION OF MRNA PROCESSINGR01GM034277 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SHARP, PHILLIP A · 1985 to 2021
$8.0M
NCI NIH HHS P01 CA042063NCI NIH HHS P30 CA014051NCI NIH HHS P30-CA14051NIGMS NIH HHS R01 GM034277NIGMS NIH HHS R01 GM34277-23
6 · The paper itself

Abstract

Deep sequencing of embryonic stem cell RNA revealed many specific internal introns that are significantly more abundant than the other introns within polyadenylated transcripts; we classified these as "detained" introns (DIs). We identified thousands of DIs, many of which are evolutionarily conserved, in human and mouse cell lines as well as the adult mouse liver. DIs can have half-lives of over an hour yet remain in the nucleus and are not subject to nonsense-mediated decay (NMD). Drug inhibition of Clk, a stress-responsive kinase, triggered rapid splicing changes for a specific subset of DIs; half showed increased splicing, and half showed increased intron detention, altering transcript pools of >300 genes. Srsf4, which undergoes a dramatic phosphorylation shift in response to Clk kinase inhibition, regulates the splicing of some DIs, particularly in genes encoding RNA processing and splicing factors. The splicing of some DIs-including those in Mdm4, a negative regulator of p53-was also altered following DNA damage. After 4 h of Clk inhibition, the expression of >400 genes changed significantly, and almost one-third of these are p53 transcriptional targets. These data suggest a widespread mechanism by which the rate of splicing of DIs contributes to the level of gene expression.

Indexed as

IntronsRNA Processing, Post-TranscriptionalRNA SplicingAnimalsDNA DamageEmbryonic Stem CellsGene Expression RegulationHumansLiverMicePhosphorylationProtein Serine-Threonine KinasesProtein-Tyrosine KinasesRNA-Binding ProteinsRNA, MessengerClk dual-specificity kinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesRNA-Binding ProteinsRNA, MessengerClk kinasedetained intronspost-transcriptional splicing

Identifiers

PMID25561496
PMCPMC4281565
OpenAlexW2166468632

What OpenQuestion holds

Textmetadata
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.