Evidence map›Paper›PMID 22343828›Full record

ReviewCellular & molecular immunology2012

Regulation of NF-κB signaling by the A20 deubiquitinase.

Noula Shembade, Edward W Harhaj

Open access · bronzeAbstract readReview
In one paragraph

Review in Cellular & molecular immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

132 citing papers in PubMed, 207 citations in OpenAlex.

  1. Innate immunity: current understandings and future perspectives.Signal transduction and targeted therapy · 2026
    Review
  2. Article
  3. Review
  4. Subtype-Independent Activation of NF-κB Signaling in Breast Cancer.International journal of molecular sciences · 2026
    Article
  5. Article
  6. Article
  7. Zinc: a metallic shield against cardiac inflammation.Metallomics : integrated biometal science · 2026
    Review
  8. Article
  9. Review
  10. Trainable computation in molecular networks.bioRxiv : the preprint server for biology · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

72 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

2 authors at 1 institution in 1 country.

Noula ShembadeDepartment of Microbiology and Immunology, Sylvester Comprehensive Cancer Center, The University of Miami, Miller School of Medicine, Miami, FL 33136, USA.
Edward W Harhaj
Sylvester Comprehensive Cancer Center · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
Tissue/Pathology CoreP01CA128115 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI GUETTOUCHE, TOUMY · 2009 to 2013
$5.6M
Mechanisms of HTLV-I Tax-mediated NF-kB activationR01CA135362 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARHAJ, EDWARD W · 2009 to 2018
$2.7M
Negative regulation of NF-kB and inflammation by TAX1BP1R01GM083143 · NIGMS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARHAJ, EDWARD W · 2009 to 2012
$1.2M
NCI NIH HHS P01 CA128115NCI NIH HHS P01CA128115NCI NIH HHS P30 CA006973NCI NIH HHS R01 CA135362NCI NIH HHS R01CA135362NIGMS NIH HHS R01 GM083143NIGMS NIH HHS R01GM083143
6 · The paper itself

Abstract

The NF-κB transcription factor is a central mediator of inflammatory and innate immune signaling pathways. Activation of NF-κB is achieved by K63-linked polyubiquitination of key signaling molecules which recruit kinase complexes that in turn activate the IκB kinase (IKK). Ubiquitination is a highly dynamic process and is balanced by deubiquitinases that cleave polyubiquitin chains and terminate downstream signaling events. The A20 deubiquitinase is a critical negative regulator of NF-κB and inflammation, since A20-deficient mice develop uncontrolled and spontaneous multi-organ inflammation. Furthermore, specific polymorphisms in the A20 genomic locus predispose humans to autoimmune disease. Recent studies also indicate that A20 is an important tumor suppressor that is inactivated in B-cell lymphomas. Therefore, targeting A20 may form the basis of novel therapies for autoimmune disease and lymphomas.

Indexed as

AnimalsAutoimmune DiseasesDNA-Binding ProteinsHumansI-kappa B KinaseImmunity, InnateIntracellular Signaling Peptides and ProteinsLymphoma, B-CellMiceMice, KnockoutNF-kappa BNuclear ProteinsSignal TransductionTumor Necrosis Factor alpha-Induced Protein 3Tumor Suppressor ProteinsUbiquitinationDNA-Binding ProteinsI-kappa B KinaseIntracellular Signaling Peptides and ProteinsNF-kappa BNuclear ProteinsTNFAIP3 protein, humanTumor Necrosis Factor alpha-Induced Protein 3Tumor Suppressor ProteinsUbiquitin-Protein Ligases

Identifiers

PMID22343828
PMCPMC3532050
OpenAlexW2034236127

What OpenQuestion holds

Textmetadata
LicenceTDM
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.