Evidence map›Paper›PMID 26086143›Full record

ReviewNature immunology2015

The diverse role of RIP kinases in necroptosis and inflammation.

John Silke, James A Rickard, Motti Gerlic

Erratum issuedOpen access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 313 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
313citing papers in PubMed, 4 pooled it
25.3field-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

313 citing papers in PubMed, 4 syntheses or guidelines pooled it, 502 citations in OpenAlex.

  1. Necroptosis in pancreatic cancer: Molecular mechanisms and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026
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  18. TNF-alpha: Roles in pathogenesis and therapeutics in cancer.The Journal of biological chemistry · 2026
    Review
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  20. Targeting PANoptosis in atherosclerosis: bridging cell death mechanisms and therapy.Apoptosis : an international journal on programmed cell death · 2026
    Review

253 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

John Silke1] The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Australia.ORCID 0000000276115774
James A Rickard1] The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia. [2] Department of Medical Biology, University of Melbourne, Parkville, Australia.
Motti GerlicDepartment of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.ORCID 0000000195181833
Walter and Eliza Hall Institute of Medical Research · AUTel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is a healthy response to infection or danger and should be rapid, specific and terminated once the threat has passed. Inflammatory diseases, where this regulation fails, cause considerable human suffering. Treatments have successfully targeted pro-inflammatory cytokines, such as tumor-necrosis factor (TNF), that directly induce genes encoding inflammatory products. Inflammatory signals, including TNF, may also directly induce caspase-independent cell death (necroptosis), which can also elicit inflammation. Necroptosis was originally defined as being dependent on the kinase RIPK1 but is now known to be dependent on RIPK3 and the pseudo-kinase MLKL. Therefore, RIPK1, RIPK3 and MLKL are potential therapeutic targets. RIPK1 and RIPK3 also directly regulate inflammatory signaling, which complicates interpretation of their function but might alter their therapeutic utility. This Review examines the role of cell death, particularly necroptosis, in inflammation, in the context of recent insights into the roles of the key necroptosis effector molecules RIPK1, RIPK3 and MLKL.

Indexed as

AnimalsCytokinesHumansInflammationModels, ImmunologicalNecrosisProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionCytokinesMLKL protein, humanProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, humanRIPK3 protein, human

Identifiers

PMID26086143
OpenAlexW1850224498

What OpenQuestion holds

Textmetadata
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.