Evidence map›Paper›PMID 27779233›Full record

ArticleScientific reports2016

MicroRNA-939 restricts Hepatitis B virus by targeting Jmjd3-mediated and C/EBPα-coordinated chromatin remodeling.

Cuncun Chen, Min Wu, Wen Zhang, Wei Lu, Min Zhang, Zhanqing Zhang, Xiaonan Zhang, Zhenghong Yuan

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

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

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  5. Dual targeting of HHeliyon · 2023
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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 2 institutions in 1 country.

Cuncun ChenInstitute of Medical Microbiology and Biomedical Sciences, Shanghai Medical College of Fudan University, Shanghai, China.
Min WuResearch Units, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Wen ZhangInstitute of Medical Microbiology and Biomedical Sciences, Shanghai Medical College of Fudan University, Shanghai, China.
Wei LuDepartment of Hepatology, Shanghai Public Health Clinical Center, Shanghai, China.
Min ZhangDepartment of Clinical Laboratory, Shanghai Public Health Clinical Center, Shanghai, China.
Zhanqing ZhangDepartment of Hepatology, Shanghai Public Health Clinical Center, Shanghai, China.
Xiaonan ZhangResearch Units, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Zhenghong YuanInstitute of Medical Microbiology and Biomedical Sciences, Shanghai Medical College of Fudan University, Shanghai, China.
Shanghai Public Health Clinical Center · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multi-layered mechanisms of virus host interaction exist for chronic hepatitis B virus (HBV) infection, which have been typically manifested at the microRNA level. Our previous study suggested that miRNA-939 (miR-939) may play a potential role in regulating HBV replication. Here we further investigated the mechanism by which miR-939 regulates HBV life cycle. We found that miR-939 inhibited the abundance of viral RNAs without direct miRNA-mRNA base pairing, but via host factors. Expression profiling and functional validation identified Jmjd3 as a target responsible for miR-939 induced anti-HBV effect. Jmjd3 appeared to enhance the transcription efficiency of HBV enhancer II/core promoter (En II) in a C/EBPα-dependent manner. However, the demethylase activity of Jmjd3 was not required in this process. Rather, Jmjd3's transactivation activity depended on its interaction with C/EBPα. This coordinated action further recruited the Brm containing SWI/SNF chromatin remodeling complex which promoted the transcription of HBV RNAs. Taken together, we propose that the miR-939-Jmjd3 axis perturbs the accessibility of En II promoter to essential nuclear factors (C/EBPα and SWI/SNF complex) therefore leading to compromised viral RNA synthesis and hence restricted viral multiplication.

Indexed as

Chromatin Assembly and DisassemblyHost-Pathogen InteractionsVirus ReplicationCCAAT-Enhancer-Binding Protein-alphaCell LineChromosomal Proteins, Non-HistoneHepatitis B virusHepatocytesHumansJumonji Domain-Containing Histone DemethylasesMicroRNAsPromoter Regions, GeneticProtein BindingRNA, ViralTranscription FactorsCCAAT-Enhancer-Binding Protein-alphaChromosomal Proteins, Non-HistoneJumonji Domain-Containing Histone DemethylasesKDM6B protein, humanMicroRNAsMIRN939 microRNA, humanRNA, ViralSWI-SNF-B chromatin-remodeling complexTranscription Factors

Identifiers

PMID27779233
PMCPMC5078794
OpenAlexW2532286598

What OpenQuestion holds

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LicenceCC BY
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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.