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PMID: 9032305 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Dominant-negative inhibitors of EBNA-1 of Epstein-Barr virus.

Journal of virology ·Vol. 71 ·No. 3 ·1997-03-00 ·Pages 1766-75

Kirchmaier AL, Sugden B

Abstract

Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA-1) is required in trans to support replication of the EBV genome once per cell cycle via the latent origin of replication, oriP. EBNA-1 can also activate transcription on binding to the family of repeats of oriP to enhance some heterologous as well as native EBV promoters. We have made and screened derivatives of EBNA-1 for the ability to act as inhibitors of wild-type EBNA-1. These derivatives lack the linking or the retention functions of EBNA-1 and were analyzed for the residual ability to activate transcription and replication. We have identified derivatives of EBNA-1 that can inhibit up to 98% of wild-type EBNA-1's activities. We have also identified one derivative of EBNA-1 with only two of EBNA-1's three linking domains which can support transcription and replication inefficiently.

MeSH Terms
DNA Replication Epstein-Barr Virus Nuclear Antigens/genetics,metabolism Herpesvirus 4, Human/physiology Mutagenesis Plasmids Promoter Regions, Genetic Recombinant Fusion Proteins/genetics,metabolism Replication Origin Transcriptional Activation Tumor Cells, Cultured
Chemicals
Epstein-Barr Virus Nuclear Antigens Recombinant Fusion Proteins
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Kirchmaier A L
McArdle Laboratory for Cancer Research, University of Wisconsin Medical School, Madison 53706, USA.
Sugden B
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Article Info
Journal
Journal of virology
Abbr.
J Virol
ISSN
0022-538X
DOI
10.1128/JVI.71.3.1766-1775.1997
Published
1997-03-00
Pages
1766-75
Language
English
Region
United States
NLM ID
0113724
PMCID
PMC191245
Subset
IM
Grants
NCI NIH HHS · CA-07175 · United States
NCI NIH HHS · CA-22443 · United States
NCI NIH HHS · T32-CA-09135 · United States
External Links
PubMed source DOI: 10.1128/JVI.71.3.1766-1775.1997 PMC Full Text View journal details
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