Evidence map›Paper›PMID 26794869›Full record

ArticleCell research2016

The kinase activity of PKR represses inflammasome activity.

Howard C H Yim, Die Wang, Liang Yu, Christine L White, Pieter W Faber, Bryan R G Williams, Anthony J Sadler

Open access · bronzeAbstract read
In one paragraph

Article in Cell research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Selective inhibition of PKR by C16 accelerates diabetic wound healing by inhibiting NALP3 expression in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  7. Article
  8. Anti‑βInternational journal of molecular medicine · 2022
    Article
  9. Article
  10. Signaling pathways and intervention therapies in sepsis.Signal transduction and targeted therapy · 2021
    Review
  11. Review
  12. Article
  13. Role of NLRP3 Inflammasome Activation in Obesity-Mediated Metabolic Disorders.International journal of environmental research and public health · 2021
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
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  20. Article
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

7 authors at 3 institutions in 2 countries.

Howard C H YimCentre for Cancer Research, Hudson Institute of Medical Research, 27-31 Wright St, Clayton, Victoria 3168, Australia.
Die WangCentre for Cancer Research, Hudson Institute of Medical Research, 27-31 Wright St, Clayton, Victoria 3168, Australia.
Liang YuCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, 27-31 Wright St, Clayton, Victoria 3168, Australia.
Christine L WhiteCentre for Cancer Research, Hudson Institute of Medical Research, 27-31 Wright St, Clayton, Victoria 3168, Australia.
Pieter W FaberChicago Genomics Facility, University of Chicago, IL 60637, USA.
Bryan R G WilliamsCentre for Cancer Research, Hudson Institute of Medical Research, 27-31 Wright St, Clayton, Victoria 3168, Australia.
Anthony J SadlerCentre for Cancer Research, Hudson Institute of Medical Research, 27-31 Wright St, Clayton, Victoria 3168, Australia.
Hudson Institute of Medical Research · AUMonash University · AUUniversity of Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The protein kinase R (PKR) functions in the antiviral response by controlling protein translation and inflammatory cell signaling pathways. We generated a transgenic, knock-in mouse in which the endogenous PKR is expressed with a point mutation that ablates its kinase activity. This novel animal allows us to probe the kinase-dependent and -independent functions of PKR. We used this animal together with a previously generated transgenic mouse that is ablated for PKR expression to determine the role of PKR in regulating the activity of the cryopyrin inflammasome. Our data demonstrate that, in contradiction to earlier reports, PKR represses cryopyrin inflammasome activity. We demonstrate that this control is mediated through the established function of PKR to inhibit protein translation of constituents of the inflammasome to prevent initial priming during innate immune signaling. These findings identify an important role for PKR to dampen inflammation during the innate immune response and caution against the previously proposed therapeutic strategy to inhibit PKR to treat inflammation.

Indexed as

AnimalseIF-2 KinaseInflammasomesInterleukin-18Interleukin-1betaMacrophagesMice, TransgenicNLR Family, Pyrin Domain-Containing 3 ProteineIF-2 KinaseInflammasomesInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseprotein kinase R, mouse

Identifiers

PMID26794869
PMCPMC4783464
OpenAlexW2319029052

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.