Evidence map›Paper›PMID 25342750›Full record

ArticleThe Journal of biological chemistry2014

MicroRNA-26b inhibits hepatitis B virus transcription and replication by targeting the host factor CHORDC1 protein.

Fanpeng Zhao, Gang Xu, Yaqin Zhou, Lvyin Wang, Jiajia Xie, Sheng Ren, Shi Liu, Ying Zhu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  6. miR‑148a‑3p regulates alcoholic liver fibrosis through targeting ERBB3.International journal of molecular medicine · 2020
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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 1 institution in 1 country.

Fanpeng ZhaoFrom the State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, Hubei, China.
Gang XuFrom the State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, Hubei, China.
Yaqin ZhouFrom the State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, Hubei, China.
Lvyin WangFrom the State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, Hubei, China.
Jiajia XieFrom the State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, Hubei, China.
Sheng RenFrom the State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, Hubei, China.
Shi LiuFrom the State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, Hubei, China.
Ying ZhuFrom the State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, Hubei, China yingzhu@whu.edu.cn.
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) causes acute and chronic hepatitis in humans, and HBV infection is a major threat to global health. HBV replication is regulated by a series of host factors, including microRNAs (miRNAs), which are highly conserved small noncoding RNAs that participate in a variety of physiological and pathological processes. Here, we report that a chemically synthesized mimic of miR-26b inhibited HBV antigen expression, transcription, and replication, whereas antisense knockdown of endogenous miR-26b enhanced HBV replication in HepG2 cells. Overexpression and knockdown experiments showed that miR-26b significantly decreased HBV enhancer/promoter activities. We identified the cysteine- and histidine-rich domain containing 1 (CHORDC1) as a novel host factor target of miR-26b. CHORDC1 protein but not mRNA was markedly decreased by miR-26b overexpression via base-pairing with complementary sequences in the 3'UTR of its mRNA. Overexpression and knockdown studies showed that CHORDC1 increased viral antigen expression, transcription, and replication by elevating HBV enhancer/promoter activities. Conversely, HBV infection suppressed miR-26b expression and increased CHORDC1 protein levels in human liver cells. Another mature miRNA of the hsa-miR-26 family, miR-26a, had a similar function as miR-26b in targeting CHORDC1 and affecting HBV production. These results suggest that suppression of miR-26b expression up-regulates its target gene CHORDC1, which increases HBV enhancer/promoter activities and promotes viral transcription, gene expression, and replication. Our study could provide new insights into miRNA expression and the persistence of HBV infection.

Indexed as

Base SequenceCarrier ProteinsEnhancer Elements, GeneticGene Expression Regulation, ViralHepatitis B virusHep G2 CellsHumansLiverMicroRNAsPhosphate-Binding ProteinsPromoter Regions, GeneticTranscription, GeneticVirus ReplicationCarrier ProteinsCHORDC1 protein, humanMicroRNAsMIRN26 microRNA, humanPhosphate-Binding ProteinsCHORDC1Hepatitis B VirusHepatitis VirusHost FactorHost-Pathogen InteractionInfectious DiseaseMicroRNA-26bMicroRNA (miRNA)Viral InfectionViral Transcription

Identifiers

PMID25342750
PMCPMC4263898
OpenAlexW2060040928

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.