Evidence map›Paper›PMID 29316268›Full record

ArticleMolecular oncology2018

Crosstalk between hepatitis B virus X and high-mobility group box 1 facilitates autophagy in hepatocytes.

Sha Fu, Juan Wang, Xingwang Hu, Rong-Rong Zhou, Yongming Fu, Daolin Tang, Rui Kang, Yan Huang, Lunquan Sun, Ning Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  3. Review
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  8. Article
  9. BAP1 forms a trimer with HMGB1 and HDAC1 that modulates gene × environment interaction with asbestos.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Article
  11. Journal of virology · 2021
    Article
  12. Autophagy in liver diseases.World journal of hepatology · 2021
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
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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

11 authors at 3 institutions in 2 countries.

Sha FuDepartment of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha, China.
Juan WangDepartment of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha, China.
Xingwang HuDepartment of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha, China.
Rong-Rong ZhouDepartment of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha, China.
Yongming FuDepartment of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha, China.
Daolin TangDepartment of Surgery, University of Pittsburgh, PA, USA.
Rui KangDepartment of Surgery, University of Pittsburgh, PA, USA.
Yan HuangDepartment of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha, China.
Lunquan SunCenter for Molecular Medicine, Xiangya Hospital, Central South University, Changsha, China.
Ning LiDepartment of Blood Transfusion, Xiangya Hospital, Central South University, Changsha, China.
Xue-Gong FanDepartment of Infectious Diseases, Hunan Key Laboratory of Viral Hepatitis, Xiangya Hospital, Central South University, Changsha, China.
Xiangya Hospital Central South University · CNCentral South University · CNUniversity of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) X (HBx) protein is a pivotal regulator of HBV-triggered autophagy. However, the role of HBx-induced epigenetic changes in autophagy remains largely unknown. The cytoplasmic (Cyt) high-mobility group box 1 (HMGB1) has been identified as a positive regulator of autophagy, and its Cyt translocation is closely associated with its acetylation status. Here, we evaluated the function of HMGB1 in HBx-mediated autophagy and its association with histone deacetylase (HDAC). Using cell lines with enforced expression of HBx, we demonstrated that HBx upregulated the expression of HMGB1 and promoted its Cyt translocation by acetylation to facilitate autophagy. We further identified the underlying mechanism by which decreased nuclear HDAC activity and expression levels contribute to the HBx-promoted hyperacetylation and subsequent translocation of HMGB1. We also identified the HDAC1 isoform as a critical factor in regulating this phenomenon. In addition, HBx bound to HMGB1 in the cytoplasm, which triggered autophagy in hepatocytes. Pharmacological inhibition of HMGB1 Cyt translocation with ethyl pyruvate prevented HBx-induced autophagy. These results demonstrate a novel function of acetylated HMGB1 in HBx-mediated autophagy in hepatocytes.

Indexed as

AutophagyAcetylationAnimalsCell LineCytoplasmGene Knockdown TechniquesHepatocytesHep G2 CellsHistone Deacetylase 1HMGB1 ProteinHumansMiceMice, Inbred C57BLPyruvatesTrans-ActivatorsViral Regulatory and Accessory Proteinsethyl pyruvateHDAC1 protein, humanhepatitis B virus X proteinHistone Deacetylase 1HMGB1 ProteinHMGB1 protein, humanPyruvatesTrans-ActivatorsViral Regulatory and Accessory Proteinsacetylationautophagyhepatitis B virushigh-mobility group box 1histone deacetylasesprotein protein interaction

Identifiers

PMID29316268
PMCPMC5830655
OpenAlexW2783994401

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.