2001
DOI: 10.1128/jvi.75.6.2584-2596.2001
|View full text |Cite
|
Sign up to set email alerts
|

Protein-DNA Binding and CpG Methylation at Nucleotide Resolution of Latency-Associated Promoters Qp, Cp, and LMP1p of Epstein-Barr Virus

Abstract: Epstein-Barr viral (EBV) latency-associated promotersEpstein-Barr virus (EBV) infection is the cause of infectious mononucleosis and is most closely associated with tumor diseases Burkitt's lymphoma (BL) and nasopharyngeal carcinoma. EBV infection of human B lymphocytes in vitro results in B-cell proliferation and transformation into continuously growing lymphoblastoid cell lines (LCL) (for a review, see reference 42). In latently infected cells, viral genomes are maintained as multiple circular episomal copie… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1

Citation Types

5
66
0

Year Published

2003
2003
2016
2016

Publication Types

Select...
4
3

Relationship

1
6

Authors

Journals

citations
Cited by 63 publications
(71 citation statements)
references
References 116 publications
5
66
0
Order By: Relevance
“…CpG methylation switches off gene expression and induces the alternative transcription of EBNA1 from various promoters in the different latency stages that, at the same time, are associated with the pathology that the virus induces, from a simple infection to a lymphoma or carcinoma (Li and Minarovits, 2003;Yoshioka et al, 2003;Niller et al, 2008). Although Wp, Cp and Fp have been found methylated in a specific latency type, Qp remains unmethylated, irrespective of its activity, and is thought to be regulated by a putative repressor protein and specific histone modifications (Tao et al, 1998;Paulson and Speck, 1999;Salamon et al, 2001;Li and Minarovits, 2003;Tao and Robertson, 2003;Minarovits, 2006;Fejer et al, 2008;Fernandez et al, 2009). …”
Section: Epstein-barr Virusmentioning
confidence: 99%
“…CpG methylation switches off gene expression and induces the alternative transcription of EBNA1 from various promoters in the different latency stages that, at the same time, are associated with the pathology that the virus induces, from a simple infection to a lymphoma or carcinoma (Li and Minarovits, 2003;Yoshioka et al, 2003;Niller et al, 2008). Although Wp, Cp and Fp have been found methylated in a specific latency type, Qp remains unmethylated, irrespective of its activity, and is thought to be regulated by a putative repressor protein and specific histone modifications (Tao et al, 1998;Paulson and Speck, 1999;Salamon et al, 2001;Li and Minarovits, 2003;Tao and Robertson, 2003;Minarovits, 2006;Fejer et al, 2008;Fernandez et al, 2009). …”
Section: Epstein-barr Virusmentioning
confidence: 99%
“…This discrepancy may be due to the different passage history of the cells used. While Cp activity is regulated by both CpG methylation (Altiok et al, 1992;Minarovits et al, 1994;Robertson et al, 1995;Salamon et al, 2001;Bakos et al, 2007) and histone modifications (this study), Qp is unmethylated independently of its activity (Tao et al, 1998;Salamon et al, 2001). We observed that similar to active Cp, active Q promoters in lymphoid and epithelial cells are also located on an acetylation island enriched in AcH3 and AcH4.…”
mentioning
confidence: 50%
“…Day et al (2007) also detected elevated H3K4me2 at Qp in the Mutu-I cells they studied, as well as in Raji cells (a BL line not known to use Qp). We suggest that Qp usage is regulated, in addition to a putative repressor protein (Salamon et al, 2001), by regional histone modifications. To our knowledge this is the first study connecting upregulation of Cp and Qp activity with a local, coordinated increase in the acetylation of histones H3 and H4.…”
mentioning
confidence: 99%
See 2 more Smart Citations