Evidence map›Paper›PMID 19074903›Full record

ArticleCancer research2008

Premature cell cycle entry induced by hepatitis B virus regulatory HBx protein during compensatory liver regeneration.

Amanda J Hodgson, Victor V Keasler, Betty L Slagle

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Cell death pathways and viruses: Role of microRNAs.Molecular therapy. Nucleic acids · 2021
    Review
  5. Review
  6. Article
  7. Article
  8. Hepatitis B Virus X and Regulation of Viral Gene Expression.Cold Spring Harbor perspectives in medicine · 2016
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Cell cycle regulation during viral infection.Methods in molecular biology (Clifton, N.J.) · 2014
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Nuclear HBx binds the HBV minichromosome and modifies the epigenetic regulation of cccDNA function.Proceedings of the National Academy of Sciences of the United States of America · 2009
    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

3 authors at 1 institution in 1 country.

Amanda J HodgsonDepartment of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA.
Victor V Keasler
Betty L Slagle
Baylor College of Medicine · US

Funding

Hepatitis HBx-Mediated PathogenesisR01CA095388 · NCI · BAYLOR COLLEGE OF MEDICINE · PI SLAGLE, BETTY L · 2003 to 2007
$1.5M
Hepatitis HBx-Mediated PathogenesisR56CA095388 · NCI · BAYLOR COLLEGE OF MEDICINE · PI SLAGLE, BETTY L · 2009 to 2009
$300k
NCI NIH HHS CA095388NCI NIH HHS R01 CA095388NCI NIH HHS R56 CA095388
6 · The paper itself

Abstract

The cycles of cell death and compensatory regeneration that occur during chronic hepatitis B virus (HBV) infection are central to viral pathogenesis and are a risk factor for the development of liver cancer. The HBV genome encodes one regulatory protein, HBx, which is required for virus replication, although its precise role in replication and pathogenesis is unclear. Because HBx can induce the G(0)-G(1) transition in cultured cells, the purpose of this study was to examine the effect of HBx during liver regeneration. Transgenic mice expressing HBx (ATX) and their wild-type (WT) littermates were used in the partial hepatectomy (PH) model for compensatory regeneration. Liver tissues collected from ATX and WT mice at varying sacrifice time points after PH were examined for markers of cell cycle progression. When compared with WT liver tissues, ATX livers had evidence of premature cell cycle entry as assessed by several variables (BrdUrd incorporation, proliferating cell nuclear antigen and mitotic indices, and reduced steady-state p21 protein levels). However, HBx did not affect apoptosis, glycogen storage, or PH-induced steatosis. Together, these results show that HBx expression can induce cell cycle progression within the regenerating liver. Our data are consistent with a model in which HBx expression contributes to liver disease and cancer formation by affecting early steps in liver regeneration.

Indexed as

AnimalsCell CycleCell DivisionDNAHepatitis B, ChronicHepatocytesLiver RegenerationLysophospholipase DMiceMice, TransgenicMultienzyme ComplexesPhosphodiesterase IPhosphoric Diester HydrolasesPyrophosphatasesTrans-ActivatorsViral Regulatory and Accessory ProteinsDNAhepatitis B virus X proteinLysophospholipase DMultienzyme ComplexesPhosphodiesterase IPhosphoric Diester HydrolasesPyrophosphatasesTrans-ActivatorsViral Regulatory and Accessory Proteins

Identifiers

PMID19074903
PMCPMC2730779
OpenAlexW2079924052

What OpenQuestion holds

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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.