Evidence map›Paper›PMID 35970851›Full record

ArticleCell death & disease2022

PKR and TLR3 trigger distinct signals that coordinate the induction of antiviral apoptosis.

Wenjie Zuo, Mai Wakimoto, Noriyasu Kozaiwa, Yutaro Shirasaka, Seong-Wook Oh, Shiori Fujiwara, Hitoshi Miyachi, Amane Kogure, Hiroki Kato, Takashi Fujita

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. 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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Wenjie ZuoDivision of Integrated Life Science, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto, 606-8507, Japan.
Mai WakimotoDivision of Integrated Life Science, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto, 606-8507, Japan.
Noriyasu KozaiwaDivision of Integrated Life Science, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto, 606-8507, Japan.
Yutaro ShirasakaDivision of Integrated Life Science, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto, 606-8507, Japan.ORCID 0000-0003-0608-8122
Seong-Wook OhLaboratory of Regulatory Information, Institute for Frontier Life and Medical Science, Kyoto University, Sakyo-ku, Kyoto, 606-8507, Japan.
Shiori FujiwaraDivision of Integrated Life Science, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto, 606-8507, Japan.
Hitoshi MiyachiInstitute for Virus Research, Kyoto University, Sakyo-ku, Kyoto, 606-8507, Japan.
Amane KogureLaboratory of Regulatory Information, Institute for Frontier Life and Medical Science, Kyoto University, Sakyo-ku, Kyoto, 606-8507, Japan.
Hiroki Kato *Institute for Cardiovascular Immunology, University Hospital Bonn, Bonn, 53127, Germany. hkato@uni-bonn.de.
Takashi Fujita *Division of Integrated Life Science, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto, 606-8507, Japan. fujita.takashi.86e@st.kyoto-u.ac.jp.ORCID 0000-0001-9961-0535
Kyoto University · JPUniversity Hospital Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RIG-I-like receptors (RLRs), protein kinase R (PKR), and endosomal Toll-like receptor 3 (TLR3) sense viral non-self RNA and are involved in cell fate determination. However, the mechanisms by which intracellular RNA induces apoptosis, particularly the role of each RNA sensor, remain unclear. We performed cytoplasmic injections of different types of RNA and elucidated the molecular mechanisms underlying viral dsRNA-induced apoptosis. The results obtained revealed that short 5'-triphosphate dsRNA, the sole ligand of RIG-I, induced slow apoptosis in a fraction of cells depending on IRF-3 transcriptional activity and IFN-I production. However, intracellular long dsRNA was sensed by PKR and TLR3, which activate distinct signals, and synergistically induced rapid apoptosis. PKR essentially induced translational arrest, resulting in reduced levels of cellular FLICE-like inhibitory protein and functioned in the TLR3/TRIF-dependent activation of caspase 8. The present results demonstrated that PKR and TLR3 were both essential for inducing the viral RNA-mediated apoptosis of infected cells and the arrest of viral production.

Indexed as

Antiviral AgentsToll-Like Receptor 3ApoptosiseIF-2 KinaseInterferon-betaRNA, Double-StrandedRNA, ViralAntiviral AgentseIF-2 KinaseInterferon-betaRNA, Double-StrandedRNA, ViralToll-Like Receptor 3

Identifiers

PMID35970851
PMCPMC9378677
OpenAlexW4291447904

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.