Evidence map›Paper›PMID 36875104›Full record

ArticleFrontiers in immunology2023

The protein kinase R modifies gut physiology to limit colitis.

Howard Chi Ho Yim, Arindam Chakrabarti, Sean Kessler, Hiroyuki Morimoto, Die Wang, Dhanya Sooraj, Afsar U Ahmed, Carol de la Motte, Robert H Silverman, Bryan Rg Williams and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

11 authors at 4 institutions in 3 countries.

Howard Chi Ho YimCentre for Cancer Research, Hudson Institute of Medical Research, Clayton, VIC, Australia.
Arindam ChakrabartiDepartment of Cancer Biology, Lerner Research Institute, Cleveland, OH, United States.
Sean KesslerDepartment of Pathobiology, Lerner Research Institute, Cleveland, OH, United States.
Hiroyuki MorimotoCentre for Cancer Research, Hudson Institute of Medical Research, Clayton, VIC, Australia.
Die WangCentre for Cancer Research, Hudson Institute of Medical Research, Clayton, VIC, Australia.
Dhanya SoorajCentre for Cancer Research, Hudson Institute of Medical Research, Clayton, VIC, Australia.
Afsar U AhmedCentre for Cancer Research, Hudson Institute of Medical Research, Clayton, VIC, Australia.
Carol de la MotteDepartment of Pathobiology, Lerner Research Institute, Cleveland, OH, United States.
Robert H SilvermanDepartment of Cancer Biology, Lerner Research Institute, Cleveland, OH, United States.
Bryan Rg WilliamsCentre for Cancer Research, Hudson Institute of Medical Research, Clayton, VIC, Australia.
Anthony J SadlerCentre for Cancer Research, Hudson Institute of Medical Research, Clayton, VIC, Australia.
Cleveland Clinic Lerner College of Medicine · USHudson Institute of Medical Research · AUMonash University · AUUniversity of Occupational and Environmental Health Japan · JP

Funding

REGULATION OF 2-5A-DEPENDENT RNASE LEVELS OF INTERFERONR01CA044059 · NCI · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI SILVERMAN, ROBERT H. · 1986 to 2015
$6.1M
ANTIVIRAL MECHANISMS OF 2-5A-DEPENDENT RNASE LR01AI135922 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI SILVERMAN, ROBERT H. · 2017 to 2021
$2.0M
Hyaluronan regulation of microbial host defense of the intestineR01HD061918 · NICHD · CLEVELAND CLINIC LERNER COM-CWRU · PI DE LA MOTTE, CAROL A. · 2009 to 2013
$2.0M
NCI NIH HHS R01 CA044059NIAID NIH HHS R01 AI135922NICHD NIH HHS R01 HD061918
6 · The paper itself

Abstract

Here we investigate the function of the innate immune molecule protein kinase R (PKR) in intestinal inflammation. To model a colitogenic role of PKR, we determine the physiological response to dextran sulfate sodium (DSS) of wild-type and two transgenic mice strains mutated to express either a kinase-dead PKR or to ablate expression of the kinase. These experiments recognize kinase-dependent and -independent protection from DSS-induced weight loss and inflammation, against a kinase-dependent increase in the susceptibility to DSS-induced injury. We propose these effects arise through PKR-dependent alteration of gut physiology, evidenced as altered goblet cell function and changes to the gut microbiota at homeostasis that suppresses inflammasome activity by controlling autophagy. These findings establish that PKR functions as both a protein kinase and a signaling molecule in instituting immune homeostasis in the gut.

Indexed as

ColitisAnimalsAutophagyHomeostasisInflammationMiceMice, TransgenicProtein KinasesProtein Kinasesautophagycolitisgoblet cellsgut barrierinflammasomesinflammationprotein kinase

Identifiers

PMID36875104
PMCPMC9981792
OpenAlexW4321241631

What OpenQuestion holds

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LicenceCC BY
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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.