Evidence map›Paper›PMID 25793935›Full record

ArticlePloS one2015

The Ras GTPase-activating protein Rasal3 supports survival of naive T cells.

Ryunosuke Muro, Takeshi Nitta, Toshiyuki Okada, Hitoshi Ideta, Takeshi Tsubata, Harumi Suzuki

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

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

6 authors at 2 institutions in 1 country.

Ryunosuke MuroDepartment of Immunology and Pathology, Research Institute, National Center for Global Health and Medicine, Ichikawa-shi, Chiba, Japan; Department of Immunology, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.
Takeshi NittaDepartment of Immunology and Pathology, Research Institute, National Center for Global Health and Medicine, Ichikawa-shi, Chiba, Japan.
Toshiyuki OkadaDepartment of Immunology and Pathology, Research Institute, National Center for Global Health and Medicine, Ichikawa-shi, Chiba, Japan.
Hitoshi IdetaDepartment of Immunology and Pathology, Research Institute, National Center for Global Health and Medicine, Ichikawa-shi, Chiba, Japan.
Takeshi TsubataDepartment of Immunology, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.
Harumi SuzukiDepartment of Immunology and Pathology, Research Institute, National Center for Global Health and Medicine, Ichikawa-shi, Chiba, Japan.
National Center for Global Health and Medicine · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Ras-mitogen-activated protein kinase (MAPK) pathway is crucial for T cell receptor (TCR) signaling in the development and function of T cells. The significance of various modulators of the Ras-MAPK pathway in T cells, however, remains to be fully understood. Ras-activating protein-like 3 (Rasal3) is an uncharacterized member of the SynGAP family that contains a conserved Ras GTPase-activating protein (GAP) domain, and is predominantly expressed in the T cell lineage. In the current study, we investigated the function and physiological roles of Rasal3. Our results showed that Rasal3 possesses RasGAP activity, but not Rap1GAP activity, and represses TCR-stimulated ERK phosphorylation in a T cell line. In systemic Rasal3-deficient mice, T cell development in the thymus including positive selection, negative selection, and β-selection was unaffected. However, the number of naive, but not effector memory CD4 and CD8 T cell in the periphery was significantly reduced in Rasal3-deficient mice, and associated with a marked increase in apoptosis of these cells. Indeed, survival of Rasal3 deficient naive CD4 T cells in vivo by adoptive transfer was significantly impaired, whereas IL-7-dependent survival of naive CD4 T cells in vitro was unaltered. Collectively, Rasal3 is required for in vivo survival of peripheral naive T cells, contributing to the maintenance of optimal T cell numbers.

Indexed as

AnimalsAntibodies, MonoclonalApoptosisCell DifferentiationCell LineCell SurvivalGene ExpressionMiceMice, KnockoutMice, TransgenicProtein Transportras GTPase-Activating ProteinsReceptors, Antigen, T-CellSignal TransductionT-LymphocytesAntibodies, MonoclonalRASAL3 protein, mouseras GTPase-Activating ProteinsReceptors, Antigen, T-Cell

Identifiers

PMID25793935
PMCPMC4368693
OpenAlexW2056353037

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.