Evidence map›Paper›PMID 22388040›Full record

ArticleNature immunology2012

NF-κB-mediated degradation of the coactivator RIP140 regulates inflammatory responses and contributes to endotoxin tolerance.

Ping-Chih Ho, Yao-Chen Tsui, Xudong Feng, David R Greaves, Li-Na Wei

Abstract read
In one paragraph

Article in Nature immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

61 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
  2. Nuclear receptor coregulator NRIP1 R448G modulates T cell gut homing to control intestinal inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. RIP140 regulatesCancer drug resistance (Alhambra, Calif.) · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Metabolic Syndrome and Skin Diseases.Frontiers in endocrinology · 2019
    Review
  20. Review

1 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

5 authors at 3 institutions in 2 countries.

Ping-Chih HoDepartment of Pharmacology, University of Minnesota Medical School, Minneapolis, Minnesota, USA.
Yao-Chen Tsui
Xudong Feng
David R Greaves
Li-Na Wei
University of Minnesota · USUniversity of Minnesota Medical Center · USUniversity of Oxford · GB

Funding

Studies of nuclear receptor corepressor, NRIP1, in vitamin A signaling pathwaysR01DK060521 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI WEI, LI-NA · 2002 to 2022
$6.9M
TR2 NUCLEAR RECEPTOR IN VITAMIN A SIGNALING PATHWAYSR01DK054733 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI WEI, LI-NA · 1999 to 2021
$5.7M
Studies of Mouse Kappa Opioid Receptor Gene RegulationR01DA011190 · NIDA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI WEI, LI-NA · 1997 to 2011
$3.3M
Studies of the Mouse Kappa Opioid Receptor GeneK02DA013926 · NIDA · UNIVERSITY OF MINNESOTA TWIN CITIES · PI WEI, LI-NA · 2002 to 2011
$1.2M
NIDA NIH HHS DA11190NIDA NIH HHS K02 DA013926NIDA NIH HHS K02-DA13926NIDA NIH HHS R01 DA011190NIDDK NIH HHS DK54733NIDDK NIH HHS DK60521NIDDK NIH HHS R01 DK054733NIDDK NIH HHS R01 DK060521
6 · The paper itself

Abstract

Tolerance to endotoxins that is triggered by prior exposure to Toll-like receptor (TLR) ligands provides a mechanism with which to dampen inflammatory cytokines. The receptor-interacting protein RIP140 interacts with the transcription factor NF-κB to regulate the expression of genes encoding proinflammatory cytokines. Here we found lipopolysaccharide stimulation of kinase Syk-mediated tyrosine phosphorylation of RIP140 and interaction of the NF-κB subunit RelA with RIP140. These events resulted in more recruitment of the E3 ligase SCF to tyrosine-phosphorylated RIP140, which degraded RIP140 to inactivate genes encoding inflammatory cytokines. Macrophages expressing nondegradable RIP140 were resistant to the establishment of endotoxin tolerance for specific 'tolerizable' genes. Our results identify RelA as an adaptor with which SCF fine tunes NF-κB target genes by targeting the coactivator RIP140 and show an unexpected role for RIP140 degradation in resolving inflammation and endotoxin tolerance.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsChromatin ImmunoprecipitationEndotoxinsGene Knockdown TechniquesImmune ToleranceImmunoblottingInflammationMiceMice, TransgenicNF-kappa BNuclear ProteinsNuclear Receptor Interacting Protein 1Signal TransductionSKP Cullin F-Box Protein LigasesUbiquitin-Protein LigasesAdaptor Proteins, Signal TransducingEndotoxinsNF-kappa BNuclear ProteinsNuclear Receptor Interacting Protein 1SKP Cullin F-Box Protein LigasesUbiquitin-Protein Ligases

Identifiers

PMID22388040
PMCPMC3309172
OpenAlexW1980266334

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.