Evidence map›Paper›PMID 11507224›Full record

ArticleJournal of virology2001

Interaction with the Epstein-Barr virus helicase targets Zta to DNA replication compartments.

G Liao, F Y Wu, S D Hayward

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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

31 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Epstein-Barr virus in systemic autoimmune diseases.Clinical & developmental immunology · 2013
    Review
  9. Article
  10. Replication of Epstein-Barr viral DNA.Cold Spring Harbor perspectives in biology · 2013
    Review
  11. Article
  12. Epstein-Barr virus and systemic lupus erythematosus.Clinical & developmental immunology · 2012
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

3 authors at 1 institution in 1 country.

G LiaoOncology Center, Johns Hopkins School of Medicine, Baltimore, Maryland 21231, USA.
F Y Wu
S D Hayward
Johns Hopkins University · US

Funding

TRAINING IN ANTICANCER DRUG DEVELOPMENTT32CA009243 · NCI · JOHNS HOPKINS UNIVERSITY · PI STIVERS, JAMES T. · 1985 to 2012
$6.2M
EBV GENOME EXPRESSION:LOCALIZATION OF SPECIFIC FUNCTIONSR01CA030356 · NCI · JOHNS HOPKINS UNIVERSITY · PI HAYWARD, S DIANE · 1986 to 2009
$3.3M
EBV GENOME EXPRESSION:LOCALIZATION OF SPECIFIC FUNCTIONSR37CA030356 · NCI · JOHNS HOPKINS UNIVERSITY · PI HAYWARD, S DIANE · 1988 to 1995
–
NCI NIH HHS CA30356NCI NIH HHS R01 CA030356NCI NIH HHS T32 CA009243NCI NIH HHS T32 CA09243
6 · The paper itself

Abstract

Zta has a dual role in the Epstein-Barr virus (EBV) lytic cycle, acting as a key regulator of EBV lytic gene expression and also being essential for lytic viral DNA replication. Zta's replication function is mediated in part through interactions with the core viral replication proteins. We now show interaction between Zta and the helicase (BBLF4) and map the binding region to within amino acids (aa) 22 to 86 of the Zta activation domain. In immunofluorescence assays, green fluorescent protein (GFP)-tagged BBLF4 localized to the cytoplasm of transfected cells. Cotransfection of Zta resulted in translocation of BBLF4-GFP into the nucleus indicating interaction between these two proteins. However, Zta with a deletion of aa 24 to 86 was unable to mediate nuclear translocation of BBLF4-GFP. Results obtained with Zta variants carrying deletions across the aa 24 to 86 region indicated more than one contact site for BBLF4 within this domain, and this was reinforced by the behavior of the four-point mutant Zta (m22/26,74/75), which was severely impaired for BBLF4 interaction. Binding of BBLF4 to Zta was confirmed using GST affinity assays. In both cotransfection-replication assays and replication assays performed in EBV-positive P3HR1 cells, the Zta (m22/26,74/75) mutant was replication defective. In Zta-transfected D98-HR1 cells, replication compartments could be detected by immunofluorescence staining using anti-BMRF1 monoclonal antibody. Cells transfected with Zta variants that were defective for helicase binding still formed replication compartments, but Zta was excluded from these compartments. These experiments reveal a role for the Zta-helicase interaction in targeting Zta to sites of viral DNA replication.

Indexed as

DNA ReplicationViral ProteinsVirus ReplicationDNA-Binding ProteinsDNA HelicasesGenes, ReporterGreen Fluorescent ProteinsHeLa CellsHerpesvirus 4, HumanHumansLuminescent ProteinsRecombinant Fusion ProteinsTrans-ActivatorsTranscriptional ActivationBZLF1 protein, Herpesvirus 4, HumanDNA-Binding ProteinsDNA HelicasesGreen Fluorescent ProteinsLuminescent ProteinsRecombinant Fusion ProteinsTrans-ActivatorsViral Proteins

Identifiers

PMID11507224
PMCPMC115124
OpenAlexW2149655243

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.