Evidence map›Paper›PMID 9687532›Full record

ArticleThe Journal of experimental medicine1998

The Vav-Rac1 pathway in cytotoxic lymphocytes regulates the generation of cell-mediated killing.

D D Billadeau, K M Brumbaugh, C J Dick, R A Schoon, X R Bustelo, P J Leibson

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 179 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

1 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

6 authors at 3 institutions in 1 country.

D D BilladeauDepartment of Immunology, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA.
K M Brumbaugh
C J Dick
R A Schoon
X R Bustelo
P J Leibson
Mayo Clinic · USStony Brook University Hospital · USState University of New York · US

Funding

MECHANISMS OF NATURAL KILLER CELL ACTIVATIONR01CA047752 · NCI · MAYO CLINIC ROCHESTER · PI BILLADEAU, DANIEL D · 1990 to 2012
$3.8M
VAV FAMILY PROTEINS IN CELL SIGNALING AND CANCERR01CA073735 · NCI · UNIVERSITY OF SALAMANCA · PI BUSTELO, XOSE R · 1997 to 2009
$1.8M
MULTIDISCIPLINARY BASIC RESEARCH TRAINING IN CANCERT32CA009441 · NCI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI SALISBURY, JEFFREY L · 1985 to 2002
$1.2M
NCI NIH HHS CA-09441NCI NIH HHS CA-47752NCI NIH HHS CA-7373501NCI NIH HHS R01 CA047752NCI NIH HHS T32 CA009441
6 · The paper itself

Abstract

The Rac1 guanine nucleotide exchange factor, Vav, is activated in hematopoietic cells in response to a large variety of stimuli. The downstream signaling events derived from Vav have been primarily characterized as leading to transcription or transformation. However, we report here that Vav and Rac1 in natural killer (NK) cells regulate the development of cell-mediated killing. There is a rapid increase in Vav tyrosine phosphorylation during the development of antibody-dependent cellular cytotoxicity and natural killing. In addition, overexpression of Vav, but not of a mutant lacking exchange factor activity, enhances both forms of killing by NK cells. Furthermore, dominant-negative Rac1 inhibits the development of NK cell-mediated cytotoxicity by two mechanisms: (a) conjugate formation between NK cells and target cells is decreased; and (b) those NK cells that do form conjugates have decreased ability to polarize their granules toward the target cell. Therefore, our results suggest that in addition to participating in the regulation of transcription, Vav and Rac1 are pivotal regulators of adhesion, granule exocytosis, and cellular cytotoxicity.

Indexed as

Cell Cycle ProteinsCytotoxicity, ImmunologicCells, CulturedGTP-Binding ProteinsGTP PhosphohydrolasesHumansKiller Cells, NaturalPhosphorylationProto-Oncogene ProteinsProto-Oncogene Proteins c-vavrac GTP-Binding ProteinsRecombinant Fusion ProteinsTyrosineCell Cycle ProteinsGTP-Binding ProteinsGTP PhosphohydrolasesProto-Oncogene ProteinsProto-Oncogene Proteins c-vavrac GTP-Binding ProteinsRecombinant Fusion ProteinsTyrosineVAV1 protein, human

Identifiers

PMID9687532
PMCPMC2212464
OpenAlexW2054697569

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.