Evidence map›Paper›PMID 10799603›Full record

ArticleJournal of virology2000

Expression of hepatitis B virus X protein does not alter the accumulation of spontaneous mutations in transgenic mice.

C R Madden, M J Finegold, B L Slagle

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.8field-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

23 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Article
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  7. Article
  8. Review
  9. Article
  10. Article
  11. Differential gene regulation by the human and mouse aryl hydrocarbon receptor.Toxicological sciences : an official journal of the Society of Toxicology · 2010
    Article
  12. Article
  13. Ah receptor represses acute-phase response gene expression without binding to its cognate response element.Laboratory investigation; a journal of technical methods and pathology · 2009
    Article
  14. Article
  15. Article
  16. Article
  17. Hepatitis B virus-induced oncogenesis.World journal of gastroenterology · 2007
    Review
  18. Review
  19. Article
  20. 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.

C R MaddenDepartment of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas 77030, USA.
M J Finegold
B L Slagle
Baylor College of Medicine · US

Funding

Research Training in Pediatrics GastroenterolgyT32DK007664 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI DOUGLAS G BURRIN · 1991 to 2026
$8.4M
HEPATITIS B VIRUS AND HEPATOCELLULAR CARCINOMAR01CA054557 · NCI · BAYLOR COLLEGE OF MEDICINE · PI SLAGLE, BETTY L · 1991 to 1999
–
NCI NIH HHS CA54557NIDDK NIH HHS T32 DK007664NIDDK NIH HHS T32DK07664
6 · The paper itself

Abstract

Chronic infection with hepatitis B virus (HBV) is one of the major etiological factors in the development of human hepatocellular carcinoma. Transgenic mice that express the HBV X protein (HBx) have previously been shown to be more sensitive to the effects of hepatocarcinogens, although the mechanism for this cofactor role remains unknown. The ability of HBx to inhibit DNA repair in transiently transfected cell lines suggests one possible pathway. In the present study, primary hepatocytes isolated from transgenic mice that possess the HBV X gene under the control of the human alpha-1-antitrypsin regulatory region (ATX mice) were found to be deficient in their ability to conduct unscheduled DNA synthesis in response to UV-induced DNA damage. In order to measure the impact of HBx expression on DNA repair in vivo, double-transgenic mice that express HBx and possess a bacteriophage lambda transgene were sacrificed at 30, 90, and 240 days of age. Mutation frequency was determined for high-molecular-weight liver DNA of ATX and control mice by functional analysis of the lambda transgene. Expression of HBx did not significantly increase the accumulation of spontaneous mutations. These results are consistent with previous studies of HBx transgenic mice in which no effect of HBx on liver histology was apparent. This new animal model provides a powerful system in which to investigate the in vivo cooperation between HBx expression and environmental carcinogens.

Indexed as

DNA DamageAnimalsApoptosisDNAFemaleHepatitis B AntigensHepatitis B, ChronicHepatitis B virusHumansLiverMaleMiceMice, Inbred C57BLMice, Inbred ICRMice, TransgenicMutagenesisDNAHepatitis B Antigenshepatitis B virus X proteinTrans-ActivatorsViral Regulatory and Accessory Proteins

Identifiers

PMID10799603
PMCPMC110881
OpenAlexW2103517190

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.