Evidence map›Paper›PMID 11581406›Full record

ArticleJournal of virology2001

DDB2 induces nuclear accumulation of the hepatitis B virus X protein independently of binding to DDB1.

A Nag, A Datta, K Yoo, D Bhattacharyya, A Chakrabortty, X Wang, B L Slagle, R H Costa, P Raychaudhuri

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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 44 citations in OpenAlex.

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  18. Expression of hepatitis B virus X protein in transgenic mice.World journal of gastroenterology · 2003
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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

9 authors at 2 institutions in 1 country.

A NagDepartment of Biochemistry and Molecular Biology, University of Illinois at Chicago, Chicago, Illinois 60612, USA.
A Datta
K Yoo
D Bhattacharyya
A Chakrabortty
X Wang
B L Slagle
R H Costa
P Raychaudhuri
University of Illinois Chicago · USBaylor College of Medicine · US

Funding

Role of DDB in Checkpoint Control and CarcinogenesisR01CA077637 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAYCHAUDHURI, PRADIP · 1999 to 2014
$3.6M
Hepatocyte Nuclear Factors in Regenerating LiverR01DK054687 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI TYNER, ANGELA L · 1999 to 2007
$2.6M
CELL CYCLE REGULATION BY THE HPV ONCOPROTEIN E7R01CA076276 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAYCHAUDHURI, PRADIP · 1999 to 2002
$346k
NCI NIH HHS CA 76276NCI NIH HHS CA 77637NCI NIH HHS R01 CA077637NIDDK NIH HHS DK 54687NIDDK NIH HHS R01 DK054687
6 · The paper itself

Abstract

The hepatitis B virus (HBV) X protein (HBx) is critical for the life cycle of the virus. HBx associates with several host cell proteins including the DDB1 subunit of the damaged-DNA binding protein DDB. Recent studies on the X protein encoded by the woodchuck hepadnavirus have provided correlative evidence indicating that the interaction with DDB1 is important for establishment of infection by the virus. In addition, the interaction with DDB1 has been implicated in the nuclear localization of HBx. Because the DDB2 subunit of DDB is required for the nuclear accumulation of DDB1, we investigated the role of DDB2 in the nuclear accumulation of HBx. Here we show that expression of DDB2 increases the nuclear levels of HBx. Several C-terminal deletion mutants of DDB2 that fail to bind DDB1 are able to associate with HBx, suggesting that DDB2 may associate with HBx independently of binding to DDB1. We also show that DDB2 enhances the nuclear accumulation of HBx independently of binding to DDB1, since a mutant that does not bind DDB1 is able to enhance the nuclear accumulation of HBx. HBV infection is associated with liver pathogenesis. We show that the nuclear levels of DDB1 and DDB2 are tightly regulated in hepatocytes. Studies with regenerating mouse liver indicate that during late G1 phase the nuclear levels of both subunits of DDB are transiently increased, followed by a sharp decrease in S phase. Taken together, these results suggest that DDB1 and DDB2 would participate in the nuclear functions of HBx effectively only during the late-G1 phase of the cell cycle.

Indexed as

Cell NucleusDNA-Binding ProteinsG1 PhaseHepatocytesHumansProtein SubunitsTrans-ActivatorsTumor Cells, CulturedViral Regulatory and Accessory ProteinsDDB1 protein, humanDdb1 protein, mouseDDB2 protein, humanDNA-Binding Proteinshepatitis B virus X proteinProtein SubunitsTrans-ActivatorsViral Regulatory and Accessory Proteins

Identifiers

PMID11581406
PMCPMC114612
OpenAlexW1980134555

What OpenQuestion holds

Textmetadata
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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.