Evidence map›Paper›PMID 19801992›Full record

ArticleNature methods2009

Engineering splicing factors with designed specificities.

Yang Wang, Cheom-Gil Cheong, Traci M Tanaka Hall, Zefeng Wang

Abstract read
In one paragraph

Article in Nature methods, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

78 citing papers in PubMed, 142 citations in OpenAlex.

  1. Article
  2. Article
  3. Strategies for programmable manipulation of alternative splicing.Current opinion in genetics & development · 2024
    Review
  4. Article
  5. Article
  6. Review
  7. Splicing Factor PQBP1 Curtails BAX Expression to Promote Ovarian Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Nuclear Aurora kinase A switches mSignal transduction and targeted therapy · 2022
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. CRISPR artificial splicing factors.Nature communications · 2020
    Article

18 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

4 authors at 2 institutions in 1 country.

Yang WangDepartment of Pharmacology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Cheom-Gil Cheong
Traci M Tanaka Hall
Zefeng Wang
National Institutes of Health · USUniversity of North Carolina at Chapel Hill · US

Funding

Structural Studies Of Post-Transcriptional Gene RegulationZIAES050165 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI HALL, TRACI M · 2009 to 2025
$45.7M
Structural Studies Of Post-transcriptional Gene RegulationZ01ES050165 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI HALL, TRACI M · 1998 to 2008
$5.0M
Modulation of VEGF-A alternative splicing as new anti-angiogenic therapeuticsR01CA158283 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WANG, ZEFENG · 2011 to 2015
$1.4M
Intramural NIH HHS Z01 ES050165NCI NIH HHS R01 CA158283
6 · The paper itself

Abstract

Alternative splicing is generally regulated by trans-acting factors that specifically bind pre-mRNA to activate or inhibit the splicing reaction. This regulation is critical for normal gene expression, and dysregulation of splicing is closely associated with human diseases. Here we engineered artificial splicing factors by combining sequence-specific RNA-binding domains of human Pumilio1 with functional domains that regulate splicing. We applied these factors to modulate different types of alternative splicing in selected targets, to examine the activity of effector domains from natural splicing factors and to modulate splicing of an endogenous human gene, Bcl-X, an anticancer target. The designer factor targeted to Bcl-X increased the amount of pro-apoptotic Bcl-xS splice isoform, thus promoting apoptosis and increasing chemosensitivity of cancer cells to common antitumor drugs. Our approach permitted the creation of artificial factors to target virtually any pre-mRNA, providing a strategy to study splicing regulation and to manipulate disease-associated splicing events.

Indexed as

Alternative SplicingAntineoplastic AgentsApoptosisbcl-X ProteinBiomedical EngineeringCell Line, TumorExonsHeLa CellsHumansProtein IsoformsRNA-Binding ProteinsRNA PrecursorsRNA SplicingTranscription FactorsAntineoplastic Agentsbcl-X ProteinProtein Isoformspumilio protein, humanRNA-Binding ProteinsRNA PrecursorsTranscription Factors

Identifiers

PMID19801992
PMCPMC2963066
OpenAlexW2060213717

What OpenQuestion holds

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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.