Evidence map›Paper›PMID 15728236›Full record

ArticleThe Journal of experimental medicine2005

An orderly inactivation of intracellular retention signals controls surface expression of the T cell antigen receptor.

Pilar Delgado, Balbino Alarcón

Abstract read
In one paragraph

Article in The Journal of experimental medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Article
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  3. Review
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  5. Review
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  7. Frontiers in cell and developmental biology · 2021
    Article
  8. Article
  9. Article
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  14. Evidence for a functional sidedness to the alphabetaTCR.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  15. Article
  16. 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

2 authors.

Pilar DelgadoCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid 28049, Spain.
Balbino Alarcón

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exit from the endoplasmic reticulum (ER) is an important checkpoint for proper assembly of multimeric plasma membrane receptors. The six subunits of the T cell receptor (TCR; TCRalpha, TCRbeta, CD3gamma, CD3delta, CD3epsilon, and CD3zeta) are each endowed with ER retention/retrieval signals, and regulation of its targeting to the plasma membrane is therefore especially intriguing. We have studied the importance of the distinct ER retention signals at different stages of TCR intracellular assembly. To this end, we have characterized first the presence of ER retention signals in CD3gamma. Despite the presence of multiple ER retention signals in CD3gamma, epsilongamma dimers reach the cell surface when the single CD3epsilon ER retention signal is deleted. Furthermore, inclusion of this CD3epsilon mutant promoted plasma membrane expression of incomplete alphabetagammaepsilon and alphabetadeltaepsilon complexes without CD3zeta. It therefore appears that the CD3epsilon ER retention signal is dominant and that it is only overridden upon the incorporation of CD3zeta. We propose that the stepwise assembly of the TCR complex guarantees that all assembly intermediates have at least one functional ER retention signal and that only a full signaling-competent TCR complex is expressed on the cell surface.

Indexed as

Signal TransductionAnimalsCD3 ComplexCell LineCell MembraneEndoplasmic ReticulumHumansMiceReceptor-CD3 Complex, Antigen, T-CellCD3 ComplexReceptor-CD3 Complex, Antigen, T-Cell

Identifiers

PMID15728236
PMCPMC2213059

What OpenQuestion holds

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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.