Evidence map›Paper›PMID 16980618›Full record

ArticleMolecular and cellular biology2006

Persistence of cooperatively stabilized signaling clusters drives T-cell activation.

Stephen C Bunnell, Andrew L Singer, David I Hong, Berri H Jacque, Martha S Jordan, Maria-Cristina Seminario, Valarie A Barr, Gary A Koretzky, Lawrence E Samelson

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing 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

68 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Pre-organized landscape of T cell surface.Frontiers in immunology · 2023
    Review
  5. Article
  6. Review
  7. Review
  8. Vav2 lacks CaJournal of cell science · 2020
    Article
  9. Review
  10. Review
  11. Cooperative assembly of a four-molecule signaling complex formed upon T cell antigen receptor activation.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

8 more citing papers are in PubMed but not listed here.

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

9 authors.

Stephen C BunnellLaboratory of Cellular and Molecular Biology, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland, USA. Stephen.Bunnell@tufts.edu
Andrew L Singer
David I Hong
Berri H Jacque
Martha S Jordan
Maria-Cristina Seminario
Valarie A Barr
Gary A Koretzky
Lawrence E Samelson

Funding

The Function of Tribbles in the Pathogenesis of AMLP01CA093615 · NCI · UNIVERSITY OF PENNSYLVANIA · PI KORETZKY, GARY A. · 2002 to 2011
$16.2M
BIOCHEMICAL BASIS OF T CELL ACTIVATIONZ01BC010304 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SAMELSON, LAWRENCE E · 1999 to 2008
$2.6M
B CELLS IN AUTOIMMUNE DIABETESF32DK009969 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SINGER, ANDREW L · 1999 to 2001
$101k
Intramural NIH HHSNCI NIH HHS P01 CA093615NCI NIH HHS P01-CA93615NIDDK NIH HHS F32 DK009969NIDDK NIH HHS F32-DK09969
6 · The paper itself

Abstract

Antigen recognition triggers the recruitment of the critical adaptor protein SLP-76 to small macromolecular clusters nucleated by the T-cell receptor (TCR). These structures develop rapidly, in parallel with TCR-induced increases in tyrosine phosphorylation and cytosolic calcium, and are likely to contribute to TCR-proximal signaling. Previously, we demonstrated that these SLP-76-containing clusters segregate from the TCR and move towards the center of the contact interface. Neither the function of these clusters nor the structural requirements governing their persistence have been examined extensively. Here we demonstrate that defects in cluster assembly and persistence are associated with defects in T-cell activation in the absence of Lck, ZAP-70, or LAT. Clusters persist normally in the absence of phospholipase C-gamma1, indicating that in the absence of a critical effector, these structures are insufficient to drive T-cell activation. Furthermore, we show that the critical adaptors LAT and Gads localize with SLP-76 in persistent clusters. Mutational analyses of LAT, Gads, and SLP-76 indicated that multiple domains within each of these proteins contribute to cluster persistence. These data indicate that multivalent cooperative interactions stabilize these persistent signaling clusters, which may correspond to the functional complexes predicted by kinetic proofreading models of T-cell activation.

Indexed as

Signal TransductionAdaptor Proteins, Signal TransducingAnimalsEnterotoxinsHumansJurkat CellsLymphocyte ActivationMembrane ProteinsMicePhosphoproteinsProtein BindingProtein Structure, TertiaryProtein TransportRecombinant Fusion ProteinsThermodynamicsT-LymphocytesAdaptor Proteins, Signal Transducingenterotoxin E, StaphylococcalEnterotoxinsLAT protein, humanMembrane ProteinsMona protein, mousePhosphoproteinsRecombinant Fusion ProteinsSLP-76 signal Transducing adaptor proteins

Identifiers

PMID16980618
PMCPMC1592897

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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.