Evidence map›Paper›PMID 27424290›Full record

ReviewTrends in immunology2016

More to Life than NF-κB in TNFR1 Signaling.

Adrian T Ting, Mathieu J M Bertrand

Open access · bronzeAbstract readReview
In one paragraph

Review in Trends in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
150citing papers in PubMed, 1 pooled it
8.4field-weighted citation impact, top 2% 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

150 citing papers in PubMed, 1 synthesis or guideline pooled it, 260 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. TNF-alpha: Roles in pathogenesis and therapeutics in cancer.The Journal of biological chemistry · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Targeting RIPK1 to modulate cell death and tumour microenvironment in cancer therapy.Journal of enzyme inhibition and medicinal chemistry · 2025
    Review
  16. Review
  17. RIPK1: A Promising Target for Intervention Neuroinflammation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Review
  18. Review
  19. Article
  20. Article

90 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 2 institutions in 2 countries.

Adrian T TingImmunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Electronic address: adrian.ting@mssm.edu.
Mathieu J M BertrandInflammation Research Center, VIB, Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, Belgium. Electronic address: mathieu.bertrand@irc.vib-ugent.be.
Icahn School of Medicine at Mount Sinai · USVIB-UGent Center for Inflammation Research · BE

Funding

THE ROLE OF ICSBP IN MUCOSAL IMMUNE RESPONSEP01DK072201 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HARPAZ, NOAM · 2006 to 2015
$14.6M
Regulation of TNF Receptor-mediated Cell DeathR01AI052417 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI TING, ADRIAN T · 2002 to 2020
$5.9M
Regulation of TNF Receptor-Mediated ApoptosisR56AI052417 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI TING, ADRIAN T · 2008 to 2008
$424k
Regulation of programmed necrosis by CYLD cleavage.R56AI104521 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI TING, ADRIAN T · 2014 to 2014
$295k
NIAID NIH HHS R01 AI052417NIAID NIH HHS R56 AI052417NIAID NIH HHS R56 AI104521NIDDK NIH HHS P01 DK072201
6 · The paper itself

Abstract

TNF is a master proinflammatory cytokine whose pathogenic role in inflammatory disorders has long been attributed to induction of proinflammatory mediators. TNF also activates cell survival and death pathways, and recent studies demonstrated that TNF also causes inflammation by inducing cell death. The default response of most cells to TNF is survival and NF-κB-mediated upregulation of prosurvival molecules is a well-documented protective mechanism downstream of TNFR1. Recent studies revealed the existence of an NF-κB-independent cell death checkpoint that restricts cell demise by inactivating RIPK1. Disruption of this checkpoint leads to RIPK1 kinase-dependent death and causes inflammation in vivo. These revelations bring complexity to the control of TNF-induced cell death, and suggest clinical benefit of RIPK1 inhibitors in TNF-driven human inflammatory disorders.

Indexed as

Signal TransductionAnimalsBiomarkersCell DeathCytokinesGene Expression RegulationHumansInflammationInflammation MediatorsNeoplasmsNF-kappa BProtein BindingProtein Processing, Post-TranslationalReceptors, Tumor Necrosis Factor, Type IBiomarkersCytokinesInflammation MediatorsNF-kappa BReceptors, Tumor Necrosis Factor, Type I

Identifiers

PMID27424290
PMCPMC5076853
OpenAlexW2474828131

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.