Evidence map›Paper›PMID 19279112›Full record

ArticleJournal of virology2009

Hepatitis B virus X protein modulates apoptosis in primary rat hepatocytes by regulating both NF-kappaB and the mitochondrial permeability transition pore.

Amy J Clippinger, Tricia L Gearhart, Michael J Bouchard

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.8field-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

51 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
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  7. The Role of Viral Proteins in the Regulation of Exosomes Biogenesis.Frontiers in cellular and infection microbiology · 2021
    Review
  8. Review
  9. Review
  10. Article
  11. [Effect and molecular mechanism of interferon-α on podocyte apoptosis induced by hepatitis B virus X protein].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
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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

3 authors at 1 institution in 1 country.

Amy J ClippingerDepartment of Biochemistry and Molecular Biology, Drexel University College of Medicine, 245 N. 15th Street, Philadelphia, PA 19102, USA.
Tricia L Gearhart
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

The hepatitis B virus (HBV) X protein (HBx) is a multifunctional protein that regulates numerous cellular signal transduction pathways, including those that modulate apoptosis. However, different HBx-dependent effects on apoptosis have been reported; these differences are likely the consequence of the exact conditions and cell types used in a study. Many of the previously reported studies that analyzed HBx regulation of apoptosis were conducted in immortalized or transformed cells, and the alterations that have transformed or immortalized these cells likely impact apoptotic pathways. We examined the effects of HBx on apoptotic pathways in cultured primary rat hepatocytes, a biologically relevant system that mimics normal hepatocytes in the liver. We analyzed the effects of HBx on apoptosis both when HBx was expressed in the absence of other HBV proteins and in the context of HBV replication. HBx stimulation of NF-kappaB inhibited the activation of apoptotic pathways in cultured primary rat hepatocytes. However, when HBx-induced activation of NF-kappaB was blocked, HBx stimulated apoptosis; blocking the activity of the mitochondrial permeability transition pore inhibited HBx activation of apoptosis. These results suggest that HBx can be either proapoptotic or antiapoptotic in hepatocytes, depending on the status of NF-kappaB, and confirm previous studies that link some HBx activities to modulation of the mitochondrial permeability transition pore. Overall, our studies define apoptotic pathways that are regulated by HBx in cultured primary hepatocytes and provide potential mechanisms for the development of HBV-associated liver cancer.

Indexed as

ApoptosisAdenoviridaeAnimalsCells, CulturedHepatitis B virusHepatocytesMaleMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreNF-kappa BRatsRats, Sprague-DawleyReassortant VirusesRNA, MessengerSignal TransductionTrans-Activatorshepatitis B virus X proteinMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreNF-kappa BRNA, MessengerTrans-ActivatorsViral Regulatory and Accessory Proteins

Identifiers

PMID19279112
PMCPMC2682098
OpenAlexW2126801776

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.