Evidence map›Paper›PMID 20400856›Full record

ArticleRNA biology

Analysis of SRrp86-regulated alternative splicing: control of c-Jun and IκBβ activity.

Amanda S Solis, James G Patton

Open access · hybridAbstract read
In one paragraph

Article in RNA biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 90% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. 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

2 authors at 2 institutions in 2 countries.

Amanda S SolisDepartment of Biological Sciences, Vanderbilt University, Nashville, TN USA.
James G Patton
Schlumberger (Ireland) · IEVanderbilt University · US

Funding

Mechanisms Regulating Alternative pre-mRNA SplicingR01GM062487 · NIGMS · VANDERBILT UNIVERSITY · PI PATTON, JAMES G. · 2002 to 2005
$1.1M
NIGMS NIH HHS R01 GM062487
6 · The paper itself

Abstract

Previous work led to the hypothesis that SRrp86, a related member of the SR protein superfamily, can interact with and modulate the activity of other SR proteins. Here, we sought to test this hypothesis by examining the effect of changing SRrp86 concentrations on overall alternative splicing patterns. SpliceArrays were used to examine 9,854 splicing events in wild-type cells, cells overexpressing SRrp86, and cells treated with siRNAs to knockdown SRrp86. From among the 500 splicing events exhibiting altered splicing under these conditions, the splicing of c-Jun and IκBβ were validated as being regulated by SRrp86 resulting in altered regulation of their downstream targets. In both cases, functionally distinct isoforms were generated that demonstrate the role SRrp86 plays in controlling alternative splicing.

Indexed as

Alternative SplicingAnimalsCell Line, TumorHeLa CellsHumansI-kappa B ProteinsMicroarray AnalysisNF-kappa BNuclear ProteinsProto-Oncogene Proteins c-junRatsRNA-Binding ProteinsRNA SplicingSerine-Arginine Splicing FactorsI kappa B beta proteinI-kappa B ProteinsNF-kappa BNuclear ProteinsProto-Oncogene Proteins c-junRNA-Binding ProteinsSerine-Arginine Splicing FactorsSREK1 protein, humanSrek1 protein, rat

Identifiers

PMID20400856
PMCPMC3070911
OpenAlexW2038103051

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.