Evidence map›Paper›PMID 10559356›Full record

ArticleJournal of virology1999

In vivo regulation of hepatitis B virus replication by peroxisome proliferators.

L G Guidotti, C M Eggers, A K Raney, S Y Chi, J M Peters, F J Gonzalez, A McLachlan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

28 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. β-Catenin Signaling Regulates theJournal of virology · 2021
    Article
  5. Article
  6. Review
  7. Article
  8. Article
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  10. Article
  11. Review
  12. Article
  13. Article
  14. Functional Characterization of Interferon Regulation Element of Hepatitis B virus Genome In Vivo.Indian journal of virology : an official organ of Indian Virological Society · 2012
    Article
  15. Article
  16. Article
  17. Article
  18. Multiple nuclear receptors may regulate hepatitis B virus biosynthesis during development.The international journal of biochemistry & cell biology · 2011
    Article
  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

7 authors at 3 institutions in 1 country.

L G GuidottiDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, California 92037, USA.
C M Eggers
A K Raney
S Y Chi
J M Peters
F J Gonzalez
A McLachlan
Scripps Research Institute · USNational Cancer Institute · USNational Institutes of Health · US

Funding

Regulation of HBV Replication by the Immune SystemR01AI040696 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI GUIDOTTI, LUCA G. · 1997 to 2012
$5.2M
REGULATION OF HEPATITIS B VIRUS TRANSCRIPTIONR01AI030070 · NIAID · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MCLACHLAN, ALAN · 1991 to 2008
$3.9M
Xenobiotic-Metabolizing EnzymesZ01BC005562 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 1996 to 2008
$1.3M
PRIMARY IMMUNODEFICIENCY DISEASE REGISTRY-266030070-266030070N01AI030070 · NIAID · PIRC, INC. · 2003 to 2005
–
NIAID NIH HHS AI40696NIAID NIH HHS N01 AI030070NIAID NIH HHS R01 AI030070NIAID NIH HHS R01 AI040696
6 · The paper itself

Abstract

The role of the peroxisome proliferator-activated receptor alpha (PPARalpha) in regulating hepatitis B virus (HBV) transcription and replication in vivo was investigated in an HBV transgenic mouse model. Treatment of HBV transgenic mice with the peroxisome proliferators Wy-14,643 and clofibric acid resulted in a less than twofold increase in HBV transcription rates and steady-state levels of HBV RNAs in the livers of these mice. In male mice, this increase in transcription was associated with a 2- to 3-fold increase in replication intermediates, whereas in female mice it was associated with a 7- to 14-fold increase in replication intermediates. The observed increases in transcription and replication were dependent on PPARalpha. HBV transgenic mice lacking this nuclear hormone receptor showed similar levels of HBV transcripts and replication intermediates as untreated HBV transgenic mice expressing PPARalpha but failed to demonstrate alterations in either RNA or DNA synthesis in response to peroxisome proliferators. Therefore, it appears that very modest alterations in transcription can, under certain circumstances, result in relatively large increases in HBV replication in HBV transgenic mice.

Indexed as

AnimalsClofibric AcidFemaleHepatitis B e AntigensHepatitis B virusHumansMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicPeroxisome ProliferatorsPyrimidinesReceptors, Cytoplasmic and NuclearTranscription FactorsTranscription, GeneticClofibric AcidHepatitis B e AntigensPeroxisome Proliferatorspirinixic acidPyrimidinesReceptors, Cytoplasmic and NuclearTranscription Factors

Identifiers

PMID10559356
PMCPMC113093
OpenAlexW2109459995

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.