Evidence map›Paper›PMID 11080163›Full record

ArticleThe EMBO journal2000

Vav-2 controls NFAT-dependent transcription in B- but not T-lymphocytes.

G M Doody, D D Billadeau, E Clayton, A Hutchings, R Berland, S McAdam, P J Leibson, M Turner

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 80 citations in OpenAlex.

  1. FcRL1, a New B-Cell-Activating Co-Receptor.International journal of molecular sciences · 2025
    Review
  2. Article
  3. Article
  4. Review
  5. Vav2 lacks CaJournal of cell science · 2020
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

8 authors at 1 institution in 1 country.

G M DoodyLymphocyte Signaling and Development Laboratory, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge CB2 4AT, UK.
D D Billadeau
E Clayton
A Hutchings
R Berland
S McAdam
P J Leibson
M Turner
Babraham Institute · GB

Funding

MECHANISMS OF NATURAL KILLER CELL ACTIVATIONR01CA047752 · NCI · MAYO CLINIC ROCHESTER · PI BILLADEAU, DANIEL D · 1990 to 2012
$3.8M
LYMPHOCYTE DEVELOPMENTR01AI015803 · NIAID · TUFTS UNIVERSITY BOSTON · PI WORTIS, HENRY H · 1985 to 2002
$805k
LYMPHOCYTE DEVELOPMENTR37AI015803 · NIAID · TUFTS UNIVERSITY BOSTON · PI WORTIS, HENRY H · 1987 to 1991
–
NCI NIH HHS CA47752NCI NIH HHS R01 CA047752NIAID NIH HHS AI15803
6 · The paper itself

Abstract

We show here that Vav-2 is tyrosine phosphorylated following antigen receptor engagement in both B- and T-cells, but potentiates nuclear factor of activated T cells (NFAT)-dependent transcription only in B cells. Vav-2 function requires the N-terminus, as well as functional Dbl homology and SH2 domains. More over, the enhancement of NFAT-dependent transcription by Vav-2 can be inhibited by a number of dominant-negative GTPases. The ability of Vav-2 to potentiate NFAT-dependent transcription correlates with its ability to promote a sustained calcium flux. Thus, Vav-2 augments the calcium signal in B cells but not T cells, and a truncated form of Vav-2 can neither activate NFAT nor augment calcium signaling. The CD19 co-receptor physically interacts with Vav-2 and synergistically enhances Vav-2 phosphorylation induced by the B-cell receptor (BCR). In addition, we found that Vav-2 augments CD19-stimulated NFAT- dependent transcription, as well as transcription from the CD5 enhancer. These data suggest a role for Vav-2 in transducing BCR signals to the transcription factor NFAT and implicate Vav-2 in the integration of BCR and CD19 signaling.

Indexed as

Nuclear ProteinsAnimalsAntigens, CD19B-LymphocytesCD5 AntigensCells, CulturedDNA-Binding ProteinsHumansJurkat CellsMiceNFATC Transcription FactorsOncogene ProteinsPhosphorylationProto-Oncogene Proteins c-vavReceptor Protein-Tyrosine KinasesReceptors, Antigen, B-CellAntigens, CD19CD5 AntigensDNA-Binding ProteinsNFATC Transcription FactorsNuclear ProteinsOncogene ProteinsProto-Oncogene Proteins c-vavReceptor Protein-Tyrosine KinasesReceptors, Antigen, B-CellTranscription FactorsTyrosineVAV2 protein, humanVav2 protein, mouse

Identifiers

PMID11080163
PMCPMC305817
OpenAlexW2170907762

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.