Evidence map›Paper›PMID 29128684›Full record

ReviewThe international journal of biochemistry & cell biology2018

MAPK p38 regulates inflammatory gene expression via tristetraprolin: Doing good by stealth.

J D O'Neil, A J Ammit, A R Clark

Open access · hybridAbstract readReview
In one paragraph

Review in The international journal of biochemistry & cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

38 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. Role of MAPK Pathways in the Pathogenesis of Vitiligo.Current issues in molecular biology · 2026
    Review
  4. Review
  5. Article
  6. The volatile oil ofFrontiers in pharmacology · 2025
    Article
  7. Shiga Toxins Produced by EnterohaemorrhagicJournal of microbiology and biotechnology · 2024
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Knockout of MAPK Phosphatase-1 Exaggerates Type I IFN Response during SystemicJournal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  19. Article
  20. Review
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 2 institutions in 2 countries.

J D O'NeilInstitute of Inflammation and Ageing, University of Birmingham, Birmingham B15 2WB, United Kingdom.
A J AmmitWoolcock Emphysema Centre, Woolcock Institute of Medical Research, University of Sydney, New South Wales, Australia; School of Life Sciences, Faculty of Science, University of Technology, Sydney, New South Wales, Australia.
A R ClarkInstitute of Inflammation and Ageing, University of Birmingham, Birmingham B15 2WB, United Kingdom. Electronic address: a.r.clark@bham.ac.uk.
University of Birmingham · GBUniversity of Sydney · AU

Funding

Medical Research Council G0800207Versus Arthritis 19614
6 · The paper itself

Abstract

Tristetraprolin (TTP) is an RNA-destabilizing protein that exerts profound anti-inflammatory effects by inhibiting the expression of tumour necrosis factor and many other inflammatory mediators. The mitogen-activated protein kinase (MAPK) p38 signaling pathway controls the strength and duration of inflammatory responses by regulating both the expression and function of TTP. The kinase MK2 (MAPK activated kinase 2) is activated by MAPK p38, and in turn phosphorylates TTP at two critical serine residues. One consequence of these phosphorylations is the protection of TTP from proteasome-mediated degradation. Another consequence is the loss of mRNA destabilizing activity. The control of TTP expression and function by the MAPK p38 pathway provides an elegant mechanism for coupling the on and off phases of inflammatory responses, and dictating the precise kinetics of expression of individual inflammatory mediators.

Indexed as

Gene Expression RegulationMAP Kinase Signaling SystemModels, ImmunologicalAnimalsEnzyme ActivationHumansImmune SystemInflammationIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2p38 Mitogen-Activated Protein KinasesPhosphorylationProteasome Endopeptidase ComplexProtein Processing, Post-TranslationalProtein Serine-Threonine KinasesProteolysisIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2p38 Mitogen-Activated Protein KinasesProteasome Endopeptidase ComplexProtein Serine-Threonine KinasesTristetraprolinAdenosine/uridine-rich elementInflammationMAPK p38Post-transcriptional regulationTristetraprolin

Identifiers

PMID29128684
PMCPMC6562201
OpenAlexW2767449807

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.