Evidence map›Paper›PMID 24589849›Full record

ArticleAutophagy2014

Hepatitis C virus core protein activates autophagy through EIF2AK3 and ATF6 UPR pathway-mediated MAP1LC3B and ATG12 expression.

Ji Wang, Rongyan Kang, He Huang, Xueyan Xi, Bei Wang, Jianwei Wang, Zhendong Zhao

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
8.6field-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

98 citing papers in PubMed, 148 citations in OpenAlex.

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  19. HCV-induced autophagy and innate immunity.Frontiers in immunology · 2024
    Review
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38 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Ji WangMOH Key Laboratory of Systems Biology of Pathogens; Institute of Pathogen Biology; Chinese Academy of Medical Sciences and Peking Union Medical College; Beijing, China.
Rongyan KangMOH Key Laboratory of Systems Biology of Pathogens; Institute of Pathogen Biology; Chinese Academy of Medical Sciences and Peking Union Medical College; Beijing, China.
He HuangMOH Key Laboratory of Systems Biology of Pathogens; Institute of Pathogen Biology; Chinese Academy of Medical Sciences and Peking Union Medical College; Beijing, China.
Xueyan XiMOH Key Laboratory of Systems Biology of Pathogens; Institute of Pathogen Biology; Chinese Academy of Medical Sciences and Peking Union Medical College; Beijing, China.
Bei WangMOH Key Laboratory of Systems Biology of Pathogens; Institute of Pathogen Biology; Chinese Academy of Medical Sciences and Peking Union Medical College; Beijing, China.
Jianwei WangMOH Key Laboratory of Systems Biology of Pathogens; Institute of Pathogen Biology; Chinese Academy of Medical Sciences and Peking Union Medical College; Beijing, China.
Zhendong ZhaoMOH Key Laboratory of Systems Biology of Pathogens; Institute of Pathogen Biology; Chinese Academy of Medical Sciences and Peking Union Medical College; Beijing, China.
Peking Union Medical College Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HCV infection induces autophagy, but how this occurs is unclear. Here, we report the induction of autophagy by the structural HCV core protein and subsequent endoplasmic reticular (ER) stress in Huh7 hepatoma cells. During ER stress, both the EIF2AK3 and ATF6 pathways of the unfolded protein response (UPR) were activated by HCV core protein. Then, these pathways upregulated transcription factors ATF4 and DDIT3. The ERN1-XBP1 pathway was not activated. Through ATF4 in the EIF2AK3 pathway, the autophagy gene ATG12 was upregulated. DDIT3 upregulated the transcription of autophagy gene MAP1LC3B (LC3B) by directly binding to the -253 to -99 base region of the LC3B promoter, contributing to the development of autophagy. Collectively, these data suggest not only a novel role for the HCV core protein in autophagy but also offer new insight into detailed molecular mechanisms with respect to HCV-induced autophagy, specifically how downstream UPR molecules regulate key autophagic gene expression.

Indexed as

Activating Transcription Factor 6AutophagyAutophagy-Related Protein 12Cells, CulturedeIF-2 KinaseGene Expression RegulationHumansMicrotubule-Associated ProteinsRNA, Small InterferingSignal TransductionSmall Ubiquitin-Related Modifier ProteinsTranscription Factor CHOPUnfolded Protein ResponseViral Core ProteinsActivating Transcription Factor 6ATF6 protein, humanATG12 protein, humanAutophagy-Related Protein 12DDIT3 protein, humanEIF2AK3 protein, humaneIF-2 KinaseMAP1LC3B protein, humanMicrotubule-Associated Proteinsnucleocapsid protein, Hepatitis C virusRNA, Small InterferingSmall Ubiquitin-Related Modifier ProteinsTranscription Factor CHOPViral Core ProteinsautophagycoreER stresshepatitis C virusUPR

Identifiers

PMID24589849
PMCPMC5119055
OpenAlexW2106409322

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.