Evidence map›Paper›PMID 27154354›Full record

ReviewJournal of leukocyte biology2016

TRAF3 as a powerful and multitalented regulator of lymphocyte functions.

Gail A Bishop

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 25% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Reduction of TRAF3 by heterozygosity or aging impacts B cell function.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Review
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  8. Article
  9. TRAF3: Guardian of T lymphocyte functions.Frontiers in immunology · 2023
    Review
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  11. Article
  12. Article
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  15. Article
  16. Review
  17. Article
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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

1 author at 1 institution in 1 country.

Gail A BishopDepartment of Microbiology, The University of Iowa, Iowa City, Iowa, USA; gail-bishop@uiowa.edu.
University of Iowa · US

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Christopher K Laubenthal · 2000 to 2026
$70.0M
The Role of Monocytes in non-Hodgkin LymphomaP50CA097274 · NCI · UNIVERSITY OF IOWA · PI LENTZ, STEVEN R · 2002 to 2021
$45.7M
Pulmonary Toxicology Facility CoreP30ES005605 · NIEHS · UNIVERSITY OF IOWA · PI Jong Sung Kim · 1990 to 2026
$40.5M
Molecular regulation of T cell activation signals by TRAF3R01AI123107 · NIAID · UNIVERSITY OF IOWA · PI BISHOP, GAIL A. · 2016 to 2020
$1.9M
NIAID NIH HHS R01 AI123107NIEHS NIH HHS P30 ES005605
6 · The paper itself

Abstract

This review summarizes the current state of knowledge regarding the roles of the signaling adapter protein tumor necrosis factor receptor (TNFR)-associated factor 3 in regulating the functions of B and T lymphocytes. In B lymphocytes, TNFR-associated factor 3 inhibits signaling by TNFR superfamily receptors, Toll-like receptors, and interleukin-6R. In contrast, signaling to B cells by the virally encoded oncogenic protein latent membrane protein 1 is promoted by TNFR-associated factor 3. An important B cell-specific role for TNFR-associated factor 3 is the inhibition of homeostatic survival, directly relevant to the common occurrence of TNFR-associated factor 3 mutations in human B cell malignancies. TNFR-associated factor 3 was recently found to be a resident nuclear protein in B cells, where it interacts with and inhibits gene expression mediated by the cAMP response element-binding protein transcription complex, including expression of the prosurvival protein myeloid leukemia cell differentiation protein 1. In T lymphocytes, TNFR-associated factor 3 is required for normal signaling by the T cell antigen receptor, while inhibiting signaling by the interleukin-2 receptor. Cytoplasmic TNFR -associated factor 3 restrains nuclear factor-κB2 activation in both T and B cells. Clinical implications and future directions for the study of this context-dependent signaling regulator are discussed.

Indexed as

AnimalsAntibody FormationB-LymphocytesCD40 AntigensCell LineCell SurvivalForecastingHumansImmunity, InnateLymphocyte SubsetsMiceMice, KnockoutNF-kappa BNuclear ProteinsProtein Kinase C-deltaReceptor-CD3 Complex, Antigen, T-CellCD40 AntigensEBV-associated membrane antigen, Epstein-Barr virusNF-kappa BNuclear ProteinsPrkcd protein, mouseProtein Kinase C-deltaReceptor-CD3 Complex, Antigen, T-CellReceptors, CytokineTNF Receptor-Associated Factor 3TRAF3 protein, humanViral Matrix ProteinsB cellsignal transductionT cell

Identifiers

PMID27154354
PMCPMC6608063
OpenAlexW2346161782

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.