Evidence map›Paper›PMID 41430687›Full record

ArticleVirology journal2025

Molecular mechanism of RBM15-mediated m6A modification in hepatitis B virus replication.

Min Ni, Bingbing Li, Lingli Wang, Shengju Ma, Kun Ma

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Virology journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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.

Min NiDepartment of Laboratory Medicine, Zhengzhou Key Laboratory for In Vitro Diagnosis of Hypertensive Disorders of Pregnancy, Third Affiliated Hospital of Zhengzhou University, No. 7, Kangfu Qian Street, Erqi District, Zhengzhou, 450052, Henan, China. Nimin03710@163.com.
Bingbing LiHenan Key Laboratory of Child Brain Injury and Henan Pediatric Clinical Research Center, Third Affiliated Hospital and Institute of Neuroscience of Zhengzhou University, Zhengzhou, 450052, China.
Lingli WangDepartment of Laboratory Medicine, Zhengzhou Key Laboratory for In Vitro Diagnosis of Hypertensive Disorders of Pregnancy, Third Affiliated Hospital of Zhengzhou University, No. 7, Kangfu Qian Street, Erqi District, Zhengzhou, 450052, Henan, China.
Shengju MaDepartment of Henan Newborn Screening Center, Third Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Kun MaDepartment of Henan Newborn Screening Center, Third Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.

Funding

Medical Science and Technology Joint construction Project of Henan Province LHGJ20210443Provincial-Ministerial Jointly Supported Youth Project of the Henan Medical Science and Technology Research Program SBGJ202403037
6 · The paper itself

Abstract

backgroundHepatitis B virus (HBV) is a major human pathogen and chronically infects over 250 million people globally. The objective of our study is to investigate the mechanism of RBM15 in HBV replication, providing novel targets for HB treatment.

methodsHuh-7 cells were treated with pHBV1.3. pHBV1.3 replication in Huh-7 cells was verified by detection of HBV RNAs, HBV pgRNA and HBx levels. The expression of RBM15, HULC and BRD4 was detected by qRT-PCR or WB. After RBM15 intervention, the effect of RBM15 on HBV replication was evaluated by detections of HBV DNA and HBV RNAs via q-PCR or qRT-PCR, HBsAg and HBeAg through ELISA. Total m6A levels were analyzed by m6A quantification. The m6A enrichment on HULC was analyzed by MeRIP. Bindings of HULC to ELAVL1, and ELAVL1 to BRD4 mRNA were examined by RIP. BRD4 stability was evaluated following actinomycin D treatment. HULC or BRD4 overexpression was combined with RBM15 inhibition to validate the mechanism. Finally, the HBV replication mouse model was established for mechanism verification.

resultsRBM15 was overexpressed during HBV replication. RBM15 inhibition suppressed HBV replication. RBM15 enhanced the m6A modification on HULC and stabilized HULC expression. HULC bound to ELAVL1 and elevated BRD4 protein expression. HULC or BRD4 overexpression partially reversed the inhibitory effect of RBM15 on HBV replication.

conclusionsRBM15 enhances HBV replication by promoting the binding of HULC to ELAVL1 through m6A modification, and increasing BRD4 expression.

Indexed as

AdenosineHepatitis B virusRNA-Binding ProteinsVirus ReplicationAnimalsBromodomain Containing ProteinsCell Cycle ProteinsHepatitis BHumansMiceRNA, ViralTranscription FactorsAdenosineBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsN-methyladenosineRNA-Binding ProteinsRNA, ViralTranscription FactorsBRD4ELAVL1Hepatitis B virus replicationlncRNA HULCm6A modificationpHBV1.3RBM15

Identifiers

PMID41430687
PMCPMC12723894

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.