Evidence map›Paper›PMID 23002147›Full record

ArticleNucleic acids research2012

Genome-wide activation of latent donor splice sites in stress and disease.

Yuval Nevo, Eyal Kamhi, Jasmine Jacob-Hirsch, Ninette Amariglio, Gideon Rechavi, Joseph Sperling, Ruth Sperling

Abstract read
In one paragraph

Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

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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

7 authors.

Yuval NevoDepartment of Genetics, The Hebrew University of Jerusalem, Jerusalem 91904, Israel.
Eyal Kamhi
Jasmine Jacob-Hirsch
Ninette Amariglio
Gideon Rechavi
Joseph Sperling
Ruth Sperling

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sequences that conform to the 5' splice site (5'SS) consensus are highly abundant in mammalian introns. Most of these sequences are preceded by at least one in-frame stop codon; thus, their use for splicing would result in pre-maturely terminated aberrant mRNAs. In normally grown cells, such intronic 5'SSs appear not to be selected for splicing. However, under heat shock conditions aberrant splicing involving such latent 5'SSs occurred in a number of specific gene transcripts. Using a splicing-sensitive microarray, we show here that stress-induced (e.g. heat shock) activation of latent splicing is widespread across the human transcriptome, thus highlighting the possibility that latent splicing may underlie certain diseases. Consistent with this notion, our analyses of data from the Gene Expression Omnibus (GEO) revealed widespread activation of latent splicing in cells grown under hypoxia and in certain cancers such as breast cancer and gliomas. These changes were found in thousands of transcripts representing a wide variety of functional groups; among them are genes involved in cell proliferation and differentiation. The GEO analysis also revealed a set of gene transcripts in oligodendroglioma, in which the level of activation of latent splicing increased with the severity of the disease.

Indexed as

RNA Splice SitesRNA SplicingAspartate CarbamoyltransferaseBreast NeoplasmsCarbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)Cell LineCell Line, TumorDihydroorotaseFemaleGenome, HumanGliomaHeat-Shock ResponseHumansNeoplasmsNonsense Mediated mRNA DecayRNA, MessengerAspartate CarbamoyltransferaseCAD trifunctional enzymeCarbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)DihydroorotaseRNA, MessengerRNA Splice Sites

Identifiers

PMID23002147
PMCPMC3510495

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Registered trials

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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.