Evidence map›Paper›PMID 7565767›Full record

ArticleMolecular and cellular biology1995

Transcriptional activation of the Epstein-Barr virus latency C promoter after 5-azacytidine treatment: evidence that demethylation at a single CpG site is crucial.

K D Robertson, S D Hayward, P D Ling, D Samid, R F Ambinder

Open access · greenAbstract readComparative Study
In one paragraph

Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
4.5field-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

62 citing papers in PubMed, 126 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Epigenetic control of the Epstein-Barr lifecycle.Current opinion in virology · 2022
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Epigenetic regulation of EBV and KSHV latency.Current opinion in virology · 2013
    Review
  20. Article

2 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

K D RobertsonDepartment of Oncology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
S D Hayward
P D Ling
D Samid
R F Ambinder
Johns Hopkins University · USJohns Hopkins Medicine · USNational Institutes of Health · US

Funding

REGULATION OF REPLICATION AND LATENCY BY EBV EBNASR01CA042245 · NCI · JOHNS HOPKINS UNIVERSITY · PI HAYWARD, S DIANE · 1986 to 2002
$871k
CHEMOTHERAPY FOR IMMUNE DESTRUCTION OF EBV TUMORSR01CA063532 · NCI · JOHNS HOPKINS UNIVERSITY · PI AMBINDER, RICHARD F. · 1994 to 1996
–
NCI NIH HHS R01 CA42245NCI NIH HHS R01 CA63532
6 · The paper itself

Abstract

The Epstein-Barr Virus (EBV) latency C promoter (Cp) is the origin of transcripts for six viral proteins. The promoter is active in lymphoblastoid B-cell lines but silent in many EBV-associated tumors and tumor cell lines. In these latter cell lines, the viral episome is hypermethylated in the vicinity of this promoter. We show that in such a cell line (Rael, a Burkitt's lymphoma line), 5-azacytidine inhibits DNA methyltransferase, brings about demethylation of EBV genomes, activates Cp transcription, and induces the expression of EBNA-2. Investigation of the phenomenon demonstrates the importance of the methylation status of a particular CpG site for the regulation of the Cp: (i) genomic sequencing shows that this site is methylated when the Cp is inactive and is not methylated when the promoter is active; (ii) methylation or transition mutation at this site abolishes complex formation with a cellular binding activity (CBF2) as determined by electrophoretic mobility shift analyses, competition binding analyses, and DNase I footprinting; and (iii) a single C --> T transition mutation at this site is associated with a marked reduction (> 50-fold) of transcriptional activity in a reporter plasmid. Thus, the CBF2 binding activity is shown to be methylation sensitive and crucial to EBNA-2-mediated activation of the Cp.

Indexed as

Virus LatencyAntigens, ViralAzacitidineBase SequenceDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA FootprintingDNA, ViralEnzyme InhibitorsEpstein-Barr Virus Nuclear AntigensGene Expression Regulation, ViralHerpesvirus 4, HumanMethylationMolecular Sequence DataPromoter Regions, GeneticRNA, MessengerAntigens, ViralAzacitidineDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA, ViralEnzyme InhibitorsEpstein-Barr Virus Nuclear AntigensRNA, Messenger

Identifiers

PMID7565767
PMCPMC230866
OpenAlexW2136218894

What OpenQuestion holds

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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.