Evidence map›Paper›PMID 25970172›Full record

ArticleScientific reports2015

Hepatitis B virus replication and sex-determining region Y box 4 production are tightly controlled by a novel positive feedback mechanism.

Jian Shang, Yuan Zheng, Xiaohong Guo, Jiayin Mo, Xueping Xie, Ying Xiong, Yingle Liu, Kailang Wu, Jianguo Wu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. 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
0.8field-weighted citation impact, top 28% 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, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Dual Role of YY1 in HPV Life Cycle and Cervical Cancer Development.International journal of molecular sciences · 2022
    Review
  5. Review
  6. Article
  7. Journal of Cancer · 2021
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

9 authors at 1 institution in 1 country.

Jian ShangState Key Laboratory of Virology and College of Life Sciences, Wuhan University, Wuhan 430072, P.R. China.
Yuan ZhengState Key Laboratory of Virology and College of Life Sciences, Wuhan University, Wuhan 430072, P.R. China.
Xiaohong GuoState Key Laboratory of Virology and College of Life Sciences, Wuhan University, Wuhan 430072, P.R. China.
Jiayin MoState Key Laboratory of Virology and College of Life Sciences, Wuhan University, Wuhan 430072, P.R. China.
Xueping XieState Key Laboratory of Virology and College of Life Sciences, Wuhan University, Wuhan 430072, P.R. China.
Ying XiongState Key Laboratory of Virology and College of Life Sciences, Wuhan University, Wuhan 430072, P.R. China.
Yingle LiuState Key Laboratory of Virology and College of Life Sciences, Wuhan University, Wuhan 430072, P.R. China.
Kailang WuState Key Laboratory of Virology and College of Life Sciences, Wuhan University, Wuhan 430072, P.R. China.
Jianguo WuState Key Laboratory of Virology and College of Life Sciences, Wuhan University, Wuhan 430072, P.R. China.
Wuhan 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. However, the mechanisms underlying HBV infection and pathogenesis remain largely unknown. The sex-determining region Y box 4 (Sox4) is a transcriptional factor, which preferentially regulates the development of various organs, tissues, and cancers. But, the role of Sox4 in viral infection and pathogenesis has not been elucidated. Here, we demonstrated that Sox4 is up-regulated by HBV, and revealed the mechanism by which HBV regulates Sox4 expression. First, HBV stimulates Sox4 expression through transcriptional factor Yin Yang 1 (YY1), which binds to Sox4 promoter to activate Sox4 transcriptional activity. Second, miR-335, miR-129-2 and miR-203 inhibit Sox4 expression by targeting its mRNA 3'UTR, while HBV suppresses the microRNAs expression, resulting in up-regulating Sox4 post-transcriptionally. Third, Sox4 protein is degraded by proteasome, while HBV surface protein (HBsAg) prevents Sox4 from degradation by directly interacting with the protein, thereby enhancing Sox4 production post-translationlly. More interestingly, HBV-activated Sox4 in turn facilitates HBV replication by direct binding to the viral genome via its HMG box. Thus, this study revealed a novel positive feedback mechanism by which Sox4 production and HBV replication are tightly correlated.

Indexed as

Gene Expression RegulationVirus ReplicationCarcinoma, HepatocellularEpigenesis, GeneticGenome, ViralHepatitis BHepatitis B virusHumansLiver NeoplasmsMAP Kinase Signaling SystemMicroRNAsProteasome Endopeptidase ComplexProtein BindingProtein Interaction Domains and MotifsSOXC Transcription FactorsTranscriptional ActivationMicroRNAsProteasome Endopeptidase ComplexSOX4 protein, humanSOXC Transcription FactorsViral ProteinsYY1 Transcription Factor

Identifiers

PMID25970172
PMCPMC4429541
OpenAlexW2269100236

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.