Evidence map›Paper›PMID 26895378›Full record

ArticleOncotarget2016

ZEB2 inhibits HBV transcription and replication by targeting its core promoter.

Qiao He, Wanyu Li, Jihua Ren, Yecai Huang, Ying Huang, Qin Hu, Juan Chen, Weixian Chen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

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  12. Dexamethasone Stimulates Hepatitis B Virus (HBV) Replication Through Autophagy.Medical science monitor : international medical journal of experimental and clinical research · 2018
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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

8 authors at 4 institutions in 1 country.

Qiao HeDepartment of Laboratory Medicine, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Wanyu LiThe Second Affiliated Hospital and The Key Laboratory of Molecular Biology of Infectious Diseases designated by The Chinese Ministry of Education, Chongqing Medical University, Chongqing, China.
Jihua RenThe Second Affiliated Hospital and The Key Laboratory of Molecular Biology of Infectious Diseases designated by The Chinese Ministry of Education, Chongqing Medical University, Chongqing, China.
Yecai HuangDepartment of Radiation Oncology, Sichuan Cancer Hospital, Chengdu, China.
Ying HuangDepartment of Infectious Diseases, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Qin HuDepartment of Laboratory Medicine, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Juan ChenThe Second Affiliated Hospital and The Key Laboratory of Molecular Biology of Infectious Diseases designated by The Chinese Ministry of Education, Chongqing Medical University, Chongqing, China.
Weixian ChenDepartment of Laboratory Medicine, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Dalian Medical University · CNChongqing Medical University · CNSichuan Cancer Hospital · CNSecond Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) infection is a major cause of liver diseases, especially liver cirrhosis and hepatocellular carcinoma. However, the interaction between host and HBV has not been fully elucidated. ZEB2 is a Smad-interacting, multi-zinc finger protein that acts as a transcription factor or repressor for several signaling pathways. This study found that the expression of ZEB2 was decreased in HBV-expressing cells. Overexpression of ZEB2 inhibited HBV DNA replicative intermediates, 3.5kb mRNA, core protein level, and the secretion of HBsAg and HBeAg. In contrast, ZEB2 knockdown promoted HBV replication. Furthermore, ZEB2 could bind to HBV core promoter and inhibit its promoter activity. Mutation at the ZEB2 binding site in HBV core promoter eradicated ZEB2-mediated inhibition of HBV replication. This study identifies ZEB2 as a novel host restriction factor that inhibits HBV replication in hepatocytes. These data may shed light on development of new antiviral strategies.

Indexed as

Cell LineHepatitis BHepatitis B virusHepatocytesHost-Pathogen InteractionsHumansPromoter Regions, GeneticTranscription, GeneticViral Core ProteinsVirus ReplicationZinc Finger E-box Binding Homeobox 2Viral Core ProteinsZEB2 protein, humanZinc Finger E-box Binding Homeobox 2HBV core promoterHBV replicationZEB2

Identifiers

PMID26895378
PMCPMC4941293
OpenAlexW2294092147

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.