Evidence map›Paper›PMID 17923691›Full record

ArticleMolecular and cellular biology2007

Protein kinase C-dependent control of Bcl-x alternative splicing.

Timothée Revil, Johanne Toutant, Lulzim Shkreta, Daniel Garneau, Philippe Cloutier, Benoit Chabot

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2007. 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
1.9field-weighted citation impact, top 15% 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, 69 citations in OpenAlex.

  1. BCL-2 and BCL-xL in Cancer: Regulation, Function, and Therapeutic Targeting.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Aberrant Bcl-x splicing in cancer: from molecular mechanism to therapeutic modulation.Journal of experimental & clinical cancer research : CR · 2021
    Review
  7. Protein Kinase C Theta Modulates PCMT1 through hnRNPL to Regulate FOXP3 Stability in Regulatory T Cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2020
    Article
  8. Computational Methods for Predicting Functions at the mRNA Isoform Level.International journal of molecular sciences · 2020
    Review
  9. Article
  10. Review
  11. miR-1266-5p and miR-185-5p Promote Cell Apoptosis in Human Prostate Cancer Cell LinesAsian Pacific journal of cancer prevention : APJCP · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
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  20. Review
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

6 authors at 1 institution in 1 country.

Timothée RevilRNA/RNP Group, Département de Microbiologie et d'Infectiologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, Québec, Canada J1H 5N4.
Johanne Toutant
Lulzim Shkreta
Daniel Garneau
Philippe Cloutier
Benoit Chabot
Université de Sherbrooke · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The alternative splicing of Bcl-x generates the proapoptotic Bcl-x(S) protein and the antiapoptotic isoform Bcl-x(L). Bcl-x splicing is coupled to signal transduction, since ceramide, hormones, and growth factors alter the ratio of the Bcl-x isoforms in different cell lines. Here we report that the protein kinase C (PKC) inhibitor and apoptotic inducer staurosporine switches the production of Bcl-x towards the x(S) mRNA isoform in 293 cells. The increase in Bcl-x(S) elicited by staurosporine likely involves signaling events that affect splicing decisions, because it requires active transcription and no new protein synthesis and is independent of caspase activation. Moreover, the increase in Bcl-x(S) is reproduced with more specific inhibitors of PKC. Alternative splicing of the receptor tyrosine kinase gene Axl is similarly affected by staurosporine in 293 cells. In contrast to the case for 293 cells, PKC inhibitors do not influence the alternative splicing of Bcl-x and Axl in cancer cell lines, suggesting that these cells have sustained alterations that uncouple splicing decisions from PKC-dependent signaling. Using minigenes, we show that an exonic region located upstream of the Bcl-x(S) 5' splice site is important to mediate the staurosporine shift in Bcl-x splicing. When transplanted to other alternative splicing units, portions of this region confer splicing modulation and responsiveness to staurosporine, suggesting the existence of factors that couple splicing decisions with PKC signaling.

Indexed as

Alternative SplicingAxl Receptor Tyrosine Kinasebcl-X ProteinCaspasesCell Line, TumorExonsHumansOncogene ProteinsProtein Kinase CProtein Kinase InhibitorsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesRegulatory Sequences, Nucleic AcidRNA PrecursorsRNA Splice SitesStaurosporineAXL protein, humanAxl Receptor Tyrosine Kinasebcl-X ProteinCaspasesOncogene ProteinsProtein Kinase CProtein Kinase InhibitorsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesRNA PrecursorsRNA Splice SitesStaurosporine

Identifiers

PMID17923691
PMCPMC2169420
OpenAlexW2171184528

What OpenQuestion holds

Textmetadata
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.