Evidence map›Paper›PMID 9091590›Full record

ArticleThe Journal of experimental medicine1997

T cell receptor (TCR) mini-gene mRNA expression regulated by nonsense codons: a nuclear-associated translation-like mechanism.

S Li, D Leonard, M F Wilkinson

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

35 citing papers in PubMed, 77 citations in OpenAlex.

  1. Stress and the nonsense-mediated RNA decay pathway.Cellular and molecular life sciences : CMLS · 2017
    Review
  2. Article
  3. Article
  4. Perturbation of thymocyte development in nonsense-mediated decay (NMD)-deficient mice.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  5. Article
  6. Article
  7. Nonsense codons trigger an RNA partitioning shift.The Journal of biological chemistry · 2009
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. A nuclear translation-like factor eIF4AIII is recruited to the mRNA during splicing and functions in nonsense-mediated decay.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

S LiDepartment of Immunology, The University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.
D Leonard
M F Wilkinson
The University of Texas MD Anderson Cancer Center · US

Funding

REGULATION OF T CELL RECEPTOR EXPRESSIONF32GM018128 · NIGMS · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI LI, SHULIN · 1996 to 1997
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REGULATION OF T-CELL RECEPTOR EXPRESSIONR01GM039586 · NIGMS · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI WILKINSON, MILES FROME · 1993 to 1996
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REGULATION OF T-CELL RECEPTOR GENE EXPRESSIONR29GM039586 · NIGMS · OREGON HEALTH AND SCIENCE UNIVERSITY · PI WILKINSON, MILES FROME · 1988 to 1992
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NIGMS NIH HHS F32 GM018128NIGMS NIH HHS GM18128NIGMS NIH HHS GM39586
6 · The paper itself

Abstract

Premature termination codons (PTCs) are known to decrease mRNA levels. Here, we report our investigation of the mechanism for this downregulation using the TCR-beta gene, which acquires PTCs as a result of programmed rearrangements that occur during normal thymic development. We found that a mini-gene version of this gene, which contains only three TCR-beta exons, exhibited efficient downregulation in response to PTCs. This demonstrates that the full coding sequence is not necessary for appropriate regulation. Mutation of the translation start AUG and a downstream in-frame AUG that displayed similarity to the Kozak consensus sequence reversed the downregulatory response to PTCs. Thus, an AUG start codon is required to define the reading frame of a PTC. Specific suppressor tRNAs also reversed the downregulatory response, strongly implicating the involvement of a translation-like process. Remarkably, the addition of suppressor tRNAs or the inactivation of the start AUGs caused a dramatic rise in the levels of PTC-bearing transcripts in the nuclear fraction prepared by two independent methods. Collectively, our results provide evidence for a codon-based surveillance mechanism associated with the nucleus that downregulates aberrant transcripts encoding potentially toxic polypeptides from nonproductively rearranged genes.

Indexed as

CodonProtein BiosynthesisTerminator Regions, GeneticTranscription, GeneticAnimalsCell NucleusDown-RegulationExonsHeLa CellsHumansMammalsMutagenesis, Site-DirectedReceptors, Antigen, T-Cell, alpha-betaRecombinant ProteinsRNA, MessengerTransfectionCodonReceptors, Antigen, T-Cell, alpha-betaRecombinant ProteinsRNA, Messenger

Identifiers

PMID9091590
PMCPMC2196228
OpenAlexW2164163807

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.