Evidence map›Paper›PMID 28515304›Full record

ArticleJournal of virology2017

Reactive Oxygen Species-Mediated c-Jun NH

Linmao Zhong, Wangqin Shu, Wangbin Dai, Bo Gao, Sidong Xiong

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
8.5field-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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
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  19. Virus, Exosome, and MicroRNA: New Insights into Autophagy.Advances in experimental medicine and biology · 2022
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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

5 authors at 2 institutions in 1 country.

Linmao ZhongInstitute for Immunobiology, Department of Immunology, Shanghai Medical College of Fudan University, Shanghai, China.
Wangqin ShuInstitute for Immunobiology, Department of Immunology, Shanghai Medical College of Fudan University, Shanghai, China.
Wangbin DaiInstitute for Immunobiology, Department of Immunology, Shanghai Medical College of Fudan University, Shanghai, China.
Bo GaoInstitute for Immunobiology, Department of Immunology, Shanghai Medical College of Fudan University, Shanghai, China gaobo@fudan.edu.cn sdxiongfd@126.com.
Sidong XiongJiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, China gaobo@fudan.edu.cn sdxiongfd@126.com.
Shanghai Medical College of Fudan University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is closely associated with the regulation of hepatitis B virus (HBV) replication. HBV X protein (HBx), a multifunctional regulator in HBV-associated biological processes, has been demonstrated to be crucial for autophagy induction by HBV. However, the molecular mechanisms of autophagy induction by HBx, especially the signaling pathways involved, remain elusive. In the present investigation, we demonstrated that HBx induced autophagosome formation independently of the class I phosphatidylinositol 3-kinase (PI3K)/AKT/mTOR signaling pathway. In contrast, the class III PI3K(VPS34)/beclin-1 pathway was revealed to be critical for HBx-induced autophagosome formation. Further study showed that HBx did not affect the level of VPS34 and beclin-1 expression but inhibited beclin-1/Bcl-2 association, and c-Jun NH2-terminal kinase (JNK) signaling was found to be important for this process. Moreover, it was found that HBx treatment led to the generation of reactive oxygen species (ROS), and inhibition of ROS activity abrogated both JNK activation and autophagosome formation. Of importance, ROS-JNK signaling was also revealed to play an important role in HBV-induced autophagosome formation and subsequent HBV replication. These data may provide deeper insight into the mechanisms of autophagy induction by HBx and help in the design of new therapeutic strategies against HBV infection.

Indexed as

AutophagyBeclin-1Class III Phosphatidylinositol 3-KinasesHepatitis B virusHep G2 CellsHumansIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesReactive Oxygen SpeciesTrans-ActivatorsViral Regulatory and Accessory ProteinsBeclin-1BECN1 protein, humanBECN2 protein, humanClass III Phosphatidylinositol 3-Kinaseshepatitis B virus X proteinIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesReactive Oxygen SpeciesTrans-ActivatorsViral Regulatory and Accessory ProteinsautophagyHBV X proteinsignaling pathwayviral replication

Identifiers

PMID28515304
PMCPMC5512237
OpenAlexW2615036268

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.