Evidence map›Paper›PMID 15583869›Full record

ArticleCellular and molecular life sciences : CMLS2004

TRAF4 functions as an intermediate of GITR-induced NF-kappaB activation.

E M Esparza, R H Arch

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. GITRL impairs the immunosuppressive function of MDSCs via PTEN-mediated signaling pathway in experimental Sjögren syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  4. Article
  5. Review
  6. Review
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  8. Review
  9. Expression and Association of Tumor Necrosis Factor Receptor Associated Factor 4 (TRAF4) in Esophageal Squamous Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. TRAF molecules in cell signaling and in human diseases.Journal of molecular signaling · 2013
    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

2 authors at 1 institution in 1 country.

E M EsparzaSchool of Medicine, Departments of Medicine and Pathology and Immunology, Washington University, 660 S. Euclid Avenue, Campus Box 8052, Saint Louis, Missouri 63110, USA.
R H Arch
Washington University in St. Louis · US

Funding

PRINCIPLES IN PULMONARY RESEARCHT32HL007317 · NHLBI · WASHINGTON UNIVERSITY · PI Steven Brody, Michael J Holtzman · 1985 to 2026
$16.1M
NHLBI NIH HHS 5 R01 HL673112-02NHLBI NIH HHS T32 HL007317
6 · The paper itself

Abstract

Members of the tumor necrosis factor receptor (TNFR) family regulate the activation, differentiation, and function of many cell types, including cells of the immune system. TNFR-associated factors (TRAFs) function as adapter molecules controlling signaling pathways triggered by TNFR family members, such as activation of nuclear factor kappaB (NF-kappaB). Despite intensive research, the function of TRAF4 in signaling pathways triggered by TNFR-related proteins remains enigmatic. Intriguingly, our functional studies indicated that TRAF4 augments NF-kappaB activation triggered by glucocorticoid-induced TNFR (GITR), a receptor expressed on T cells, B cells, and macrophages. Further analyses revealed that TRAF4-mediated NF-kappaB activation downstream of GITR depends on a previously mapped TRAF-binding site in the cytoplasmic domain of the receptor and is inhibited by the cytoplasmic protein A20. GITR is thought to inhibit the suppressive function of regulatory T cells (Treg cells) and to promote activation of T cells. Taken together, our studies provide the first indications that TRAF4 elaborates GITR signaling and suggest that TRAF4 can modulate the suppressive functions of Treg cells.

Indexed as

Binding SitesCells, CulturedDNA-Binding ProteinsGene Expression RegulationHumansIntracellular Signaling Peptides and ProteinsMutationNF-kappa BNuclear ProteinsProteinsReceptors, Nerve Growth FactorTNF Receptor-Associated Factor 2TNF Receptor-Associated Factor 4Tumor Necrosis Factor alpha-Induced Protein 3Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsNF-kappa BNuclear ProteinsProteinsReceptors, Nerve Growth FactorTNFAIP3 protein, humanTNF Receptor-Associated Factor 2TNF Receptor-Associated Factor 4TRAF4 protein, humanTumor Necrosis Factor alpha-Induced Protein 3Tumor Necrosis Factor Receptor-Associated Peptides and Proteins

Identifiers

PMID15583869
PMCPMC11924440
OpenAlexW2073973721

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.