Evidence map›Paper›PMID 11158574›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2001

Caspase-2 pre-mRNA alternative splicing: Identification of an intronic element containing a decoy 3' acceptor site.

J Coté, S Dupuis, Z Jiang, J Y Wu

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
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  5. Review
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  9. Article
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  11. Article
  12. Caspases and cancer.Cell death and differentiation · 2011
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Up-regulation of the proapoptotic caspase 2 splicing isoform by a candidate tumor suppressor, RBM5.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  18. Article
  19. Article
  20. Article
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 1 institution in 2 countries.

J CotéDepartment of Pediatrics and Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA.
S Dupuis
Z Jiang
J Y Wu
Washington University in St. Louis · US

Funding

Pre-mRNA Splicing Defects and Retinal DegenerationR01EY014576 · NEI · VANDERBILT UNIVERSITY · PI WU, JANE Y · 2004 to 2008
$1.8M
Slit Signaling in Breast CancerR01CA114197 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI WU, JANE Y · 2006 to 2010
$1.3M
Alternative splicing regulation of caspase-2 geneR01GM070967 · NIGMS · VANDERBILT UNIVERSITY · PI WU, JANE Y · 2005 to 2008
$939k
NCI NIH HHS R01 CA114197NEI NIH HHS R01 EY014576NIGMS NIH HHS R01 GM070967
6 · The paper itself

Abstract

We have established a model system using the caspase-2 pre-mRNA and initiated a study on the role of alternative splicing in regulation of programmed cell death. A caspase-2 minigene construct has been made that can be alternatively spliced in transfected cells and in nuclear extracts. Using this system, we have identified a 100-nt region in downstream intron 9 that inhibits the inclusion of the 61-bp alternative exon. This element (In100) can facilitate exon skipping in the context of competing 3' or 5' splice sites, but not in single-intron splicing units. The In100 element is also active in certain heterologous pre-mRNAs, although in a highly context-dependent manner. Interestingly, we found that In100 contains a sequence that highly resembles a bona fide 3' splice site. We provide evidence that this sequence acts as a "decoy" acceptor site that engages in U2 snRNP-dependent but nonproductive splicing complexes with the 5' splice site of exon 9, hence conferring competitive advantage to the exon-skipping splicing event (E8-E10). These results reveal a mechanism of action for a negative intronic regulatory element and uncover a role for U2 snRNP in the regulation of alternative splicing.

Indexed as

Alternative Splicing3' Untranslated RegionsApoptosisBase SequenceCaspase 2CaspasesCell LineCell NucleusExonsGenes, SyntheticHeLa CellsHumansIntronsMolecular Sequence DataMutagenesis, Site-DirectedRecombinant Proteins3' Untranslated RegionsCaspase 2CaspasesRecombinant ProteinsRibonucleoprotein, U1 Small NuclearRibonucleoprotein, U2 Small NuclearRNA Precursors

Identifiers

PMID11158574
PMCPMC14688
OpenAlexW2043558295

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.