Evidence map›Paper›PMID 17923690›Full record

ArticleMolecular and cellular biology2007

RasGRF2, a guanosine nucleotide exchange factor for Ras GTPases, participates in T-cell signaling responses.

Sergio Ruiz, Eugenio Santos, Xosé R Bustelo

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.5field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
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  3. Review
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  6. Review
  7. Regulation of the Small GTPase Ras and Its Relevance to Human Disease.Methods in molecular biology (Clifton, N.J.) · 2021
    Review
  8. Article
  9. Article
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  11. Human Endogenous Retrovirus-K HML-2 integration withinProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  12. Article
  13. Article
  14. RasGRF Couples Nox4-Dependent Endoplasmic Reticulum Signaling to Ras.Arteriosclerosis, thrombosis, and vascular biology · 2017
    Article
  15. Article
  16. Article
  17. Review
  18. Review
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  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

3 authors at 1 institution in 1 country.

Sergio RuizCentro de Investigación del Cáncer and Instituto de Biología Molecular y Celular del Cáncer, CSIC-University of Salamanca, Campus Unamuno, E-37007 Salamanca, Spain.
Eugenio Santos
Xosé R Bustelo
Consejo Superior de Investigaciones Científicas · ES

Funding

VAV FAMILY PROTEINS IN CELL SIGNALING AND CANCERR01CA073735 · NCI · UNIVERSITY OF SALAMANCA · PI BUSTELO, XOSE R · 1997 to 2009
$1.8M
NCI NIH HHS 5R01-CA73735-10NCI NIH HHS R01 CA073735
6 · The paper itself

Abstract

The Ras pathway is critical for the development and function of T lymphocytes. The stimulation of this GTPase in T cells occurs primarily through the Vav1- and phospholipase C-gamma1-dependent activation of RasGRP1, a diacylglycerol-responsive Ras GDP/GTP exchange factor. Here, we show that a second exchange factor, RasGRF2, also participates in T-cell signaling. RasGRF2 is expressed in T cells, translocates to immune synapses, activates Ras, and stimulates the transcriptional factor NF-AT (nuclear factor of activated T cells) through Ras- and phospholipase C-gamma1-dependent routes. T-cell receptor-, Vav1-, and Ca2+-elicited pathways synergize with RasGRF2 for NF-AT stimulation. The analysis of RasGRF2-deficient mice indicates that this protein is required for the induction of bona fide NF-AT targets such as the cytokines tumor necrosis factor alpha and interleukin 2, while it plays minor roles in Ras activation itself. The comparison of lymphocytes from Vav1-/-, Rasgrf2-/-, and Vav1-/-; Rasgrf2-/- mice demonstrates that the RasGRF2 pathway cooperates with the Vav1/RasGRP1 route in the blasting transformation and proliferation of mature T cells. These results identify RasGRF2 as an additional component of the signaling machinery involved in T-cell receptor- and NF-AT-mediated immune responses.

Indexed as

Signal TransductionAnimalsCalciumCell DivisionCell ProliferationGene Expression RegulationHumansJurkat CellsLymphocyte ActivationMiceNFATC Transcription FactorsPhospholipase C gammaProto-Oncogene Proteins c-vavras Guanine Nucleotide Exchange Factorsras ProteinsRatsCalciumNFATC Transcription FactorsPhospholipase C gammaProto-Oncogene Proteins c-vavRASGRF2 protein, humanRasgrf2 protein, mouseras Guanine Nucleotide Exchange Factorsras ProteinsReceptors, Antigen, T-CellVav1 protein, mouse

Identifiers

PMID17923690
PMCPMC2169177
OpenAlexW2111239857

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.