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Multiple EBNA1-binding sites within oriPI are required for EBNA1-dependent transactivation of the Epstein-Barr virus C promoter.

Artikel i vetenskaplig tidskrift
Författare Henrik Zetterberg
Cecilia Boreström
Tina Nilsson
Lars Rymo
Publicerad i International journal of oncology
Volym 25
Nummer/häfte 3
Sidor 693-6
ISSN 1019-6439
Publiceringsår 2004
Publicerad vid Institutionen för laboratoriemedicin, Avdelningen för klinisk kemi/transfusionsmedicin
Sidor 693-6
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Binding Sites, Enhancer Elements (Genetics), genetics, Epstein-Barr Virus Nuclear Antigens, genetics, metabolism, Herpesvirus 4, Human, genetics, Promoter Regions (Genetics), genetics, Replication Origin, Trans-Activation (Genetics)
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

The transactivating function of the oriPI-EBNA1 complex is essential for activation of the Epstein-Barr virus (EBV) C promoter (Cp) in lymphoblastoid cell lines expressing the viral growth programme. Furthermore, the oriPI-EBNA1 complex is believed to play an important role during promoter switching upon primary infection of B-lymphocytes and establishment of latent infection in vivo. Previously, it was shown that six EBNA1-binding sites within oriPI were required for transactivation of the heterologous thymidine kinase promoter. Here, we define the number of EBNA1-binding sites within oriPI necessary for its biological function as EBNA1-dependent Cp enhancer. We show that four EBNA1-binding sites within oriPI lead to significant upregulation of Cp in response to EBNA1 and eight or more to full activation. Thus, multiple EBNA1 homodimers at oriPI are required for the formation of a transcriptionally active Cp complex, a process that involves EBNA1-induced changes in the chromatin structure including DNA looping and nucleosome destabilization.

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