Activation domain requirements for disruption of Epstein-Barr virus latency by ZEBRA.
AUTOR(ES)
Asković, S
RESUMO
Latent infection of B lymphocytes by Epstein-Barr virus (EBV) can be disrupted by expression of the EBV ZEBRA protein. ZEBRA, a transcriptional activator, initiates the EBV lytic cascade by activating viral gene expression. ZEBRA is also indispensable for viral replication and binds directly to the EBV lytic origin of replication. The studies described herein demonstrate that the activation domain. ZEBRA activation can be replaced by a heterologous acidic, proline-rich, or glutamine-rich activation domain. ZEBRA activation domain swap constructs retain ZEBRA's native abilities to activate specific EBV promoters, to disrupt EBV latency, and to stimulate replication at the EBV lytic origin. Additional work, employing sequential and internal deletions of ZEBRA's N-terminal activation domain, indicates that its separate activities are not attributable to specific subdomains but are spread throughout its N terminus and therefore cannot be inactivated by deleting localized regions.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=191931Documentos Relacionados
- Transcriptional synergy by the Epstein-Barr virus transactivator ZEBRA.
- Viral proteins associated with the Epstein-Barr virus transactivator, ZEBRA.
- Disruption of Epstein-Barr Virus Latency in the Absence of Phosphorylation of ZEBRA by Protein Kinase C
- Alteration of a single serine in the basic domain of the Epstein-Barr virus ZEBRA protein separates its functions of transcriptional activation and disruption of latency.
- Cyclic AMP-responsive element-dependent activation of Epstein-Barr virus zebra promoter by human herpesvirus 6.
