Evidence map›Paper›PMID 31189710›Full record

ArticleJournal of virology2019

Japanese Encephalitis Virus Induces Apoptosis and Encephalitis by Activating the PERK Pathway.

Qianruo Wang, Xiu Xin, Ting Wang, Jiawu Wan, Yangtao Ou, Zibing Yang, Qijia Yu, Liting Zhu, Yunli Guo, Yinsheng Wu and 6 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

53 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
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  3. Molecular Mechanisms of Cadmium-Induced Apoptosis in Fish Cells: A Review.International journal of molecular sciences · 2026
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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

16 authors at 4 institutions in 1 country.

Qianruo Wang *Institute of Pathogenic Microorganism and College of Bioscience and Engineering, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Xiu Xin *Institute of Pathogenic Microorganism and College of Bioscience and Engineering, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Ting Wang *Institute of Pathogenic Microorganism and College of Bioscience and Engineering, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Jiawu WanInstitute of Pathogenic Microorganism and College of Bioscience and Engineering, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Yangtao OuInstitute of Pathogenic Microorganism and College of Bioscience and Engineering, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Zibing YangInstitute of Pathogenic Microorganism and College of Bioscience and Engineering, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Qijia YuInstitute of Pathogenic Microorganism and College of Bioscience and Engineering, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Liting ZhuInstitute of Pathogenic Microorganism and College of Bioscience and Engineering, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Yunli GuoInstitute of Pathogenic Microorganism and College of Bioscience and Engineering, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Yinsheng WuState Key Laboratory of Biocatalysis and Enzyme Engineering, School of Life Sciences, Hubei University, Wuhan, Hubei, China.
Zhen DingKey Laboratory for Animal Health of Jiangxi Province, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Yanni ZhangJiangxi Province Center for Disease Control and Prevention, Nanchang, Jiangxi, China.
Zishu PanState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, Hubei, China.
Yuxin Tang *Key Laboratory for Animal Health of Jiangxi Province, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Shanshan Li *State Key Laboratory of Biocatalysis and Enzyme Engineering, School of Life Sciences, Hubei University, Wuhan, Hubei, China shl@hubu.edu.cn lingbaok@mail.jxau.edu.cn.
Lingbao Kong *Institute of Pathogenic Microorganism and College of Bioscience and Engineering, Jiangxi Agricultural University, Nanchang, Jiangxi, China shl@hubu.edu.cn lingbaok@mail.jxau.edu.cn.
Jiangxi Agricultural University · CNHubei University · CNNanchang Center for Disease Control and Prevention · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulated evidence demonstrates that Japanese encephalitis virus (JEV) infection triggers endoplasmic reticulum (ER) stress and neuron apoptosis. ER stress sensor protein kinase R-like endoplasmic reticulum kinase (PERK) has been reported to induce apoptosis under acute or prolonged ER stress. However, the precise role of PERK in JEV-induced apoptosis and encephalitis remains unknown. Here, we report that JEV infection activates the PERK-ATF4-CHOP apoptosis pathway both

Indexed as

Activating Transcription Factor 4AdenineAnimalsApoptosisBinding SitesCell LineDisease Models, AnimaleIF-2 KinaseEncephalitis, JapaneseEncephalitis Virus, JapaneseEndoplasmic Reticulum StressEukaryotic Initiation Factor-2IndolesMiceNeuronsProtein Multimerization7-methyl-5-(1-((3-(trifluoromethyl)phenyl)acetyl)-2,3-dihydro-1H-indol-5-yl)-7H-pyrrolo(2,3-d)pyrimidin-4-amineActivating Transcription Factor 4AdenineAtf4 protein, mouseDdit3 protein, mouseeIF-2 KinaseEukaryotic Initiation Factor-2IndolesNS4B protein, flavivirusTranscription Factor CHOPViral Nonstructural ProteinsapoptosisER stressJapanese encephalitis virusNS4BPERK

Identifiers

PMID31189710
PMCPMC6694805
OpenAlexW2952368038

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.