Evidence map›Paper›PMID 17576688›Full record

ArticleNucleic acids research2007

SR protein-mediated inhibition of CFTR exon 9 inclusion: molecular characterization of the intronic splicing silencer.

Emanuele Buratti, Cristiana Stuani, Greta De Prato, Francisco E Baralle

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

37 citing papers in PubMed, 55 citations in OpenAlex.

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  14. Diverse regulation of 3' splice site usage.Cellular and molecular life sciences : CMLS · 2015
    Review
  15. Article
  16. Review
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  18. Isolated pseudo-RNA-recognition motifs of SR proteins can regulate splicing using a noncanonical mode of RNA recognition.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  19. Article
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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

4 authors at 1 institution in 1 country.

Emanuele BurattiInternational Centre for Genetic Engineering and Biotechnology (ICGEB) 34012 Trieste, Italy.
Cristiana Stuani
Greta De Prato
Francisco E Baralle
International Centre for Genetic Engineering and Biotechnology · IT

Funding

Telethon GGP06147
6 · The paper itself

Abstract

The intronic splicing silencer (ISS) of CFTR exon 9 promotes exclusion of this exon from the mature mRNA. This negative influence has important consequences with regards to human pathologic events, as lack of exon 9 correlates well with the occurrence of monosymptomatic and full forms of CF disease. We have previously shown that the ISS element interacts with members of the SR protein family. In this work, we now provide the identification of SF2/ASF and SRp40 as the specific SR proteins binding to this element and map their precise binding sites in IVS9. We have also performed a functional analysis of the ISS element using a variety of unrelated SR-binding sequences and different splicing systems. Our results suggest that SR proteins mediate CFTR exon 9 exclusion by providing a 'decoy' sequence in the vicinity of its suboptimal donor site. The results of this study give an insight on intron 'exonization' mechanisms and provide useful indications for the development of novel therapeutic strategies aimed at the recovery of exon inclusion.

Indexed as

IntronsRegulatory Sequences, Ribonucleic AcidRNA SplicingBase SequenceBinding SitesCell Line, TumorCystic Fibrosis Transmembrane Conductance RegulatorExonsHeLa CellsHumansMolecular Sequence DataNuclear ProteinsOligonucleotides, AntisenseRNA-Binding ProteinsSerine-Arginine Splicing FactorsCystic Fibrosis Transmembrane Conductance RegulatorNuclear ProteinsOligonucleotides, AntisenseRegulatory Sequences, Ribonucleic AcidRNA-Binding ProteinsSerine-Arginine Splicing Factors

Identifiers

PMID17576688
PMCPMC1935002
OpenAlexW2103010054

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.