Evidence map›Paper›PMID 11287574›Full record

ArticleJournal of virology2001

Hepatitis B virus HBx protein activation of cyclin A-cyclin-dependent kinase 2 complexes and G1 transit via a Src kinase pathway.

M Bouchard, S Giannakopoulos, E H Wang, N Tanese, R J Schneider

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.2field-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

40 citing papers in PubMed, 88 citations in OpenAlex.

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  13. Cell cycle regulation during viral infection.Methods in molecular biology (Clifton, N.J.) · 2014
    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

5 authors at 2 institutions in 1 country.

M BouchardDepartment of Microbiology, NYU School of Medicine, New York, New York 10016, USA.
S Giannakopoulos
E H Wang
N Tanese
R J Schneider
New York University · USUniversity of Washington · US

Funding

Viral and Cellular Determinants of Hepatitis B Virus PathogenesisR01CA056533 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SCHNEIDER, ROBERT JAY · 1992 to 2011
$4.6M
HBX PROTEIN AND HEPATITIS B VIRUS INFECTIONF32CA074476 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BOUCHARD, MICHAEL J. · 1998 to 2000
$39k
BIOCHEMICAL ANALYSIS OF FACTORS ASSOCIATED WITH TFIIDR01GM051314 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI TANESE, NAOKO · 1995 to 1999
–
NCI NIH HHS CA56533NCI NIH HHS F32 CA074476NCI NIH HHS R01 CA056533NIGMS NIH HHS GM51314
6 · The paper itself

Abstract

Numerous studies have demonstrated that the hepatitis B virus HBx protein stimulates signal transduction pathways and may bind to certain transcription factors, particularly the cyclic AMP response element binding protein, CREB. HBx has also been shown to promote early cell cycle progression, possibly by functionally replacing the TATA-binding protein-associated factor 250 (TAF(II)250), a transcriptional coactivator, and/or by stimulating cytoplasmic signal transduction pathways. To understand the basis for early cell cycle progression mediated by HBx, we characterized the molecular mechanism by which HBx promotes deregulation of the G0 and G1 cell cycle checkpoints in growth-arrested cells. We demonstrate that TAF(II)250 is absolutely required for HBx activation of the cyclin A promoter and for promotion of early cell cycle transit from G0 through G1. Thus, HBx does not functionally replace TAF(II)250 for transcriptional activity or for cell cycle progression, in contrast to a previous report. Instead, HBx is shown to activate the cyclin A promoter, induce cyclin A-cyclin-dependent kinase 2 complexes, and promote cycling of growth-arrested cells into G1 through a pathway involving activation of Src tyrosine kinases. HBx stimulation of Src kinases and cyclin gene expression was found to force growth-arrested cells to transit through G1 but to stall at the junction with S phase, which may be important for viral replication.

Indexed as

CDC2-CDC28 KinasesTATA-Binding Protein Associated FactorsTranscription Factor TFIIDCell CycleCell NucleusCell SurvivalCyclin ACyclin-Dependent Kinase 2Cyclin-Dependent KinasesCytoplasmDNA-Binding ProteinsG1 PhaseHepatitis B virusHistone AcetyltransferasesHumansNuclear ProteinsCDC2-CDC28 KinasesCDK2 protein, humanCyclin ACyclin-Dependent Kinase 2Cyclin-Dependent KinasesDNA-Binding Proteinshepatitis B virus X proteinHistone AcetyltransferasesNuclear ProteinsProtein Serine-Threonine Kinasessrc-Family KinasesTATA-binding protein associated factor 250 kDaTATA-Binding Protein Associated FactorsTrans-ActivatorsTranscription Factor TFIIDViral Regulatory and Accessory Proteins

Identifiers

PMID11287574
PMCPMC114170
OpenAlexW2131334619

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.