Evidence map›Paper›PMID 18840686›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2008

Up-regulation of the proapoptotic caspase 2 splicing isoform by a candidate tumor suppressor, RBM5.

Kazuo Fushimi, Payal Ray, Amar Kar, Lei Wang, Leslie C Sutherland, Jane Y Wu

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

73 citing papers in PubMed, 142 citations in OpenAlex.

  1. RNA splicing in health and disease.Molecular biomedicine · 2026
    Review
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13 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

6 authors at 3 institutions in 2 countries.

Kazuo FushimiDepartment of Neurology, Center for Genetic Medicine, Northwestern University Feinberg School of Medicine, 303 East Superior Street, Chicago, IL 60611, USA.
Payal Ray
Amar Kar
Lei Wang
Leslie C Sutherland
Jane Y Wu
Northwestern University · USRobert H. Lurie Comprehensive Cancer Center of Northwestern UniversitySudbury Regional Hospital · CA

Funding

Pre-mRNA Splicing Defects and Retinal DegenerationR01EY014576 · NEI · VANDERBILT UNIVERSITY · PI WU, JANE Y · 2004 to 2008
$1.8M
Signal Transduction of the Netrin PathwayR01CA107193 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI WU, JANE Y · 2005 to 2009
$1.4M
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 CA107193NCI NIH HHS R01 CA114197NEI NIH HHS EY014576NEI NIH HHS R01 EY014576NIGMS NIH HHS GM070967NIGMS NIH HHS R01 GM070967
6 · The paper itself

Abstract

Similar to many genes involved in programmed cell death (PCD), the caspase 2 (casp-2) gene generates both proapoptotic and antiapoptotic isoforms by alternative splicing. Using a yeast RNA-protein interaction assay, we identified RBM5 (also known as LUCA-15) as a protein that binds to casp-2 pre-mRNA. In both transfected cells and in vitro splicing assay, RBM5 enhances the formation of proapoptotic Casp-2L. RBM5 binds to a U/C-rich sequence immediately upstream of the previously identified In100 splicing repressor element. Our mutagenesis experiments demonstrate that RBM5 binding to this intronic sequence regulates the ratio of proapoptotic/antiapoptotic casp-2 splicing isoforms, suggesting that casp-2 splicing regulation by RBM5 may contribute to its tumor suppressor activity. Our work has uncovered a player in casp-2 alternative splicing regulation and revealed a link between the alternative splicing regulator and the candidate tumor suppressor gene. Together with previous studies, our work suggests that splicing control of cell death genes may be an important aspect in tumorigenesis. Enhancing the expression or activities of splicing regulators that promote the production of proapoptotic splicing isoforms might provide a therapeutic approach to cancer.

Indexed as

Alternative SplicingApoptosis Regulatory ProteinsBinding SitesCaspase 2Cell Cycle ProteinsCell LineCysteine EndopeptidasesDNA-Binding ProteinsHumansNeoplasmsProtein BindingProtein IsoformsRNA-Binding ProteinsRNA PrecursorsTumor Suppressor ProteinsUp-RegulationApoptosis Regulatory ProteinsCASP2 protein, humanCaspase 2Cell Cycle ProteinsCysteine EndopeptidasesDNA-Binding ProteinsProtein IsoformsRBM5 protein, humanRNA-Binding ProteinsRNA PrecursorsTumor Suppressor Proteins

Identifiers

PMID18840686
PMCPMC2572934
OpenAlexW2158051523

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.