Evidence map›Paper›PMID 15613535›Full record

ArticleRNA (New York, N.Y.)2005

Nonsense-associated alternative splicing of T-cell receptor beta genes: no evidence for frame dependence.

Fabio Mohn, Marc Bühler, Oliver Mühlemann

Open access · bronzeAbstract read
In one paragraph

Article in RNA (New York, N.Y.), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

3 authors at 1 institution in 1 country.

Fabio MohnInstitute of Cell Biology, University of Bern, Baltzerstrasse 4, CH-3012 Bern, Switzerland.
Marc Bühler
Oliver Mühlemann
University of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations that generate premature translation-termination codons (PTCs) often result in production of alternatively spliced mRNAs. While in many cases, the PTC-causing mutation was found to affect splicing directly by disrupting an exonic splicing enhancer, induction of alternative splicing of TCR-beta pre-mRNA has been reported to be specific for mutations that prematurely terminate the open reading frame. During testing of a cyto-nuclear feedback model that would have explained how cytoplasmic translation could influence nuclear splicing of TCR-beta transcripts, control experiments questioned the frame dependence of the nonsense-associated altered splicing (NAS) of TCR-beta pre-mRNA. A subsequent detailed analysis of alternatively spliced TCR-beta mRNA expressed from different minigene constructs with nonsense, silent, or frame-shift mutations at various positions revealed no correlation between truncation of the reading frame and production of alternatively spliced mRNA. Our study thus contradicts the previously reported PTC specificity of TCR-beta NAS and points out the need for systematically testing the PTC specificity in other cases where NAS has been observed.

Indexed as

Alternative SplicingCell LineCodon, NonsenseFrameshift MutationGene ExpressionHeLa CellsHumansOpen Reading FramesReceptors, Antigen, T-Cell, alpha-betaReverse Transcriptase Polymerase Chain ReactionRibonucleasesRNA PrecursorsTransfectionCodon, NonsenseReceptors, Antigen, T-Cell, alpha-betaRibonucleasesRNA Precursors

Identifiers

PMID15613535
PMCPMC1370704
OpenAlexW2105840727

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.