Evidence map›Paper›PMID 34269817›Full record

ReviewThe Biochemical journal2021

Inhibitory feedback control of NF-κB signalling in health and disease.

Jack A Prescott, Jennifer P Mitchell, Simon J Cook

Open access · hybridAbstract readReview
In one paragraph

Review in The Biochemical journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed, 1 pooled it
10.9field-weighted citation impact, top 1% 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

111 citing papers in PubMed, 1 synthesis or guideline pooled it, 171 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. TPx Protein ofPathogens (Basel, Switzerland) · 2026
    Article
  5. cGAS-STING as a Neuroimmune Traffic Molecule: Unraveling Pathogenic Mechanisms and Therapeutic Potential in Neurological Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Subtype-Independent Activation of NF-κB Signaling in Breast Cancer.International journal of molecular sciences · 2026
    Article
  12. Review
  13. Article
  14. The research progress of ferroptosis in acute lung injury.Biochemistry and biophysics reports · 2026
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

51 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

3 authors at 1 institution in 1 country.

Jack A Prescott
Jennifer P MitchellSignalling Programme, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, U.K.
Simon J CookSignalling Programme, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, U.K.ORCID 0000-0001-9087-1616
Babraham Institute · GB

Funding

Biotechnology and Biological Sciences Research Council BB/S017062/1
6 · The paper itself

Abstract

Cells must adapt to changes in their environment to maintain cell, tissue and organismal integrity in the face of mechanical, chemical or microbiological stress. Nuclear factor-κB (NF-κB) is one of the most important transcription factors that controls inducible gene expression as cells attempt to restore homeostasis. It plays critical roles in the immune system, from acute inflammation to the development of secondary lymphoid organs, and also has roles in cell survival, proliferation and differentiation. Given its role in such critical processes, NF-κB signalling must be subject to strict spatiotemporal control to ensure measured and context-specific cellular responses. Indeed, deregulation of NF-κB signalling can result in debilitating and even lethal inflammation and also underpins some forms of cancer. In this review, we describe the homeostatic feedback mechanisms that limit and 're-set' inducible activation of NF-κB. We first describe the key components of the signalling pathways leading to activation of NF-κB, including the prominent role of protein phosphorylation and protein ubiquitylation, before briefly introducing the key features of feedback control mechanisms. We then describe the array of negative feedback loops targeting different components of the NF-κB signalling cascade including controls at the receptor level, post-receptor signalosome complexes, direct regulation of the critical 'inhibitor of κB kinases' (IKKs) and inhibitory feedforward regulation of NF-κB-dependent transcriptional responses. We also review post-transcriptional feedback controls affecting RNA stability and translation. Finally, we describe the deregulation of these feedback controls in human disease and consider how feedback may be a challenge to the efficacy of inhibitors.

Indexed as

Feedback, PhysiologicalSignal TransductionAnimalsCell SurvivalGene Expression RegulationHumansI-kappa B KinaseInflammationNF-kappa BPhosphorylationRNA StabilityI-kappa B KinaseNF-kappa Bdecoy receptorsdeubiquitylasesfeedbackIKKsIκBsnuclear factor κB

Identifiers

PMID34269817
PMCPMC8286839
OpenAlexW3181781482

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.