Evidence map›Paper›PMID 18448529›Full record

ArticleJournal of virology2008

Hepatitis B virus HBx protein localizes to mitochondria in primary rat hepatocytes and modulates mitochondrial membrane potential.

Amy J Clippinger, Michael J Bouchard

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Antioxidants and Calcium Modulators Preclude in Vitro Hepatitis B Virus-Induced Mitochondrial Damage.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023
    Article
  10. Relevance of HBx for Hepatitis B Virus-Associated Pathogenesis.International journal of molecular sciences · 2023
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

5 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Amy J ClippingerGraduate Program in Molecular and Cellular Biology and Genetics, Drexel University College of Medicine, Philadelphia, Pennsylvania 19102, USA.
Michael J Bouchard
Drexel University · US

Funding

Role of Hepatitis B virus X protein in HBV replication.R01AI064844 · NIAID · DREXEL UNIVERSITY · PI BOUCHARD, MICHAEL J. · 2006 to 2010
$1.6M
Hepatitis B Virus X Protein and Alcohol Regulation of Mitochondria and ApoptosisF31AA016865 · NIAAA · DREXEL UNIVERSITY · PI CLIPPINGER, AMY J · 2007 to 2008
$58k
NIAAA NIH HHS F31 AA016865NIAAA NIH HHS F31AA016865NIAID NIH HHS R01 AI064844NIAID NIH HHS R01AI064844
6 · The paper itself

Abstract

Over 350 million people are chronically infected with hepatitis B virus (HBV), and a significant number of chronically infected individuals develop primary liver cancer. HBV encodes seven viral proteins, including the nonstructural X (HBx) protein. The results of studies with immortalized or transformed cells and with HBx-transgenic mice demonstrated that HBx can interact with mitochondria. However, no studies with normal hepatocytes have characterized the precise mitochondrial localization of HBx or the effect of HBx on mitochondrial physiology. We have used cultured primary rat hepatocytes as a model system to characterize the mitochondrial localization of HBx and the effect of HBx expression on mitochondrial physiology. We now show that a fraction of HBx colocalizes with density-gradient-purified mitochondria and associates with the outer mitochondrial membrane. We also demonstrate that HBx regulates mitochondrial membrane potential in hepatocytes and that this function of HBx varies depending on the status of NF-kappaB activity. In primary rat hepatocytes, HBx activation of NF-kappaB prevented mitochondrial membrane depolarization; however, when NF-kappaB activity was inhibited, HBx induced membrane depolarization through modulation of the mitochondrial permeability transition pore. Collectively, these results define potential pathways through which HBx may act in order to modulate mitochondrial physiology, thereby altering many cellular activities and ultimately contributing to the development of HBV-associated liver cancer.

Indexed as

AnimalsBlotting, WesternCell FractionationCell LineCells, CulturedElectrophoresis, Polyacrylamide GelHepatitis B virusHepatocytesMembrane Potential, MitochondrialMitochondriaMitochondrial MembranesNF-kappa BPermeabilityRatsTrans-ActivatorsViral Regulatory and Accessory Proteinshepatitis B virus X proteinNF-kappa BTrans-ActivatorsViral Regulatory and Accessory Proteins

Identifiers

PMID18448529
PMCPMC2446973
OpenAlexW2151088538

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.