Evidence map›Paper›PMID 22956543›Full record

ArticleJournal of cell science2012

Mechanism and function of Vav1 localisation in TCR signalling.

Olga Ksionda, Alexander Saveliev, Robert Köchl, Jonathan Rapley, Mustapha Faroudi, Jennifer E Smith-Garvin, Christoph Wülfing, Katrin Rittinger, Tom Carter, Victor L J Tybulewicz

Open access · hybridAbstract read
In one paragraph

Article in Journal of cell science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. International journal of environmental research and public health · 2020
    Article
  8. Vav2 lacks CaJournal of cell science · 2020
    Article
  9. Article
  10. T Cell Reprogramming Against Cancer.Methods in molecular biology (Clifton, N.J.) · 2020
    Review
  11. Plant microRNAs fromFrontiers in pharmacology · 2020
    Article
  12. Review
  13. Article
  14. Article
  15. SYK expression in monomorphic epitheliotropic intestinal T-cell lymphoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018
    Article
  16. [Regulatory effect of Vav1 on T cells and its relation to clinical diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018
    Review
  17. Article
  18. Systems Imaging of the Immune Synapse.Methods in molecular biology (Clifton, N.J.) · 2017
    Article
  19. Article
  20. 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

10 authors at 2 institutions in 1 country.

Olga KsiondaDivision of Immune Cell Biology, MRC National Institute for Medical Research, London NW7 1AA, UK.
Alexander Saveliev
Robert Köchl
Jonathan Rapley
Mustapha Faroudi
Jennifer E Smith-Garvin
Christoph Wülfing
Katrin Rittinger
Tom Carter
Victor L J Tybulewicz
The University of Texas Southwestern Medical Center · USUniversity of Pennsylvania · US

Funding

Medical Research Council MC_U117527252Medical Research Council MC_U117565398Medical Research Council MC_U117573808Medical Research Council U117527252Medical Research Council U117565398Medical Research Council U117573808Wellcome TrustWellcome Trust 089185
6 · The paper itself

Abstract

The antigen-specific binding of T cells to antigen presenting cells results in recruitment of signalling proteins to microclusters at the cell-cell interface known as the immunological synapse (IS). The Vav1 guanine nucleotide exchange factor plays a critical role in T cell antigen receptor (TCR) signalling, leading to the activation of multiple pathways. We now show that it is recruited to microclusters and to the IS in primary CD4(+) and CD8(+) T cells. Furthermore, we show that this recruitment depends on the SH2 and C-terminal SH3 (SH3(B)) domains of Vav1, and on phosphotyrosines 112 and 128 of the SLP76 adaptor protein. Biophysical measurements show that Vav1 binds directly to these residues on SLP76 and that efficient binding depends on the SH2 and SH3(B) domains of Vav1. Finally, we show that the same two domains are critical for the phosphorylation of Vav1 and its signalling function in TCR-induced calcium flux. We propose that Vav1 is recruited to the IS by binding to SLP76 and that this interaction is critical for the transduction of signals leading to calcium flux.

Indexed as

AnimalsCalciumCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCells, CulturedHumansImmunological SynapsesMiceMutant ProteinsPhosphorylationProtein TransportProto-Oncogene Proteins c-vavReceptors, Antigen, T-CellSignal Transductionsrc Homology DomainsCalciumMutant ProteinsProto-Oncogene Proteins c-vavReceptors, Antigen, T-CellVav1 protein, mouse

Identifiers

PMID22956543
PMCPMC3561853
OpenAlexW2016012447

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.