Evidence map›Paper›PMID 31427374›Full record

ReviewCold Spring Harbor perspectives in biology2020

Multitasking Kinase RIPK1 Regulates Cell Death and Inflammation.

Kim Newton

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
–field-weighted citation impact
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

52 citing papers in PubMed, 97 citations in OpenAlex.

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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

1 author.

Kim NewtonDepartment of Physiological Chemistry, Genentech, South San Francisco, California 94080, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Receptor-interacting serine threonine kinase 1 (RIPK1) is a widely expressed kinase that is essential for limiting inflammation in both mice and humans. Mice lacking RIPK1 die at birth from multiorgan inflammation and aberrant cell death, whereas humans lacking RIPK1 are immunodeficient and develop very early-onset inflammatory bowel disease. In contrast to complete loss of RIPK1, inhibiting the kinase activity of RIPK1 genetically or pharmacologically prevents cell death and inflammation in several mouse disease models. Indeed, small molecule inhibitors of RIPK1 are in phase I clinical trials for amyotrophic lateral sclerosis, and phase II clinical trials for psoriasis, rheumatoid arthritis, and ulcerative colitis. This review focuses on which signaling pathways use RIPK1, how activation of RIPK1 is regulated, and when activation of RIPK1 appears to be an important driver of inflammation.

Indexed as

Cell DeathGene Expression RegulationGene Expression Regulation, EnzymologicAnimalsApoptosisCaspase 8Cell SurvivalClinical Trials as TopicHumansInflammationIntestinesMiceNeoplasmsPhosphorylationReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionCaspase 8Receptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, humanToll-Like Receptor 3Toll-Like Receptor 4

Identifiers

PMID31427374
PMCPMC7050590
OpenAlexW2969708224

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.