Evidence map›Paper›PMID 21914724›Full record

ArticleNucleic acids research2012

Activation and repression functions of an SR splicing regulator depend on exonic versus intronic-binding position.

Manli Shen, William Mattox

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Tumor-promoting effect and tumor immunity of SRSFs.Frontiers in cell and developmental biology · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Perspective in Alternative Splicing Coupled to Nonsense-Mediated mRNA Decay.International journal of molecular sciences · 2020
    Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  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

2 authors at 1 institution in 1 country.

Manli ShenDepartment of Genetics and Genes & Development Graduate Program, University of Texas MD Anderson Cancer Center, Houston, TX 77030-4009, USA.
William Mattox
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Positive and Negative control of pre-mRNA processingR01GM070892 · NIGMS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MATTOX, WILLIAM W · 2005 to 2010
$1.2M
NCI NIH HHS CA016672NCI NIH HHS P30 CA016672NIGMS NIH HHS GM070892
6 · The paper itself

Abstract

SR proteins and related factors play widespread roles in alternative pre-mRNA splicing and are known to promote splice site recognition through their Arg-Ser-rich effector domains. However, binding of SR regulators to some targets results in repression of splice sites through a distinct mechanism. Here, we investigate how activated and repressed targets of the Drosophila SR regulator Transformer2 elicit its differing effects on splicing. We find that, like activation, repression affects early steps in the recognition of splice sites and spliceosome assembly. Repositioning of regulatory elements reveals that Tra2 complexes that normally repress splicing from intronic positions activate splicing when located in an exon. Protein tethering experiments demonstrate that this position dependence is an intrinsic property of Tra2 and further show that repression and activation are mediated by separate effector domains of this protein. When other Drosophila SR factors (SF2 and Rbp1) that activate splicing from exonic positions were tethered intronically they failed to either activate or repress splicing. Interestingly, both activities of Tra2 favor the exonic identity of the RNA sequences that encompass its binding sites. This suggests a model in which these two opposite functions act in concert to define both the position and extent of alternatively spliced exons.

Indexed as

Alternative SplicingExonsIntronsAnimalsCells, CulturedDrosophila ProteinsRegulatory Sequences, Ribonucleic AcidRibonucleoproteinsRNA-Binding ProteinsRNA Splicing FactorsSpliceosomesDrosophila ProteinsRBP1 protein, DrosophilaRegulatory Sequences, Ribonucleic AcidRibonucleoproteinsRNA-Binding ProteinsRNA Splicing FactorsSF2 protein, Drosophilatra2 protein, Drosophila

Identifiers

PMID21914724
PMCPMC3245930
OpenAlexW2032275001

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.