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Functional Replacement of the Intracellular Region of the Notch1 Receptor by Epstein-Barr Virus Nuclear Antigen 2

By Takashi Sakai, Yoshihito Taniguchi, Kumiko Tamura, Shigeru Minoguchi, Takataro Fukuhara, Lothar J. Strobl, Ursula Zimber-Strobl, George W. Bornkamm and Tasuku Honjo

Abstract

The intracellular region (RAMIC) of the mouse Notch1 receptor interacts with RBP-J/CBF-1, which binds to the DNA sequence CGTGGGAA and suppresses differentiation by transcriptional activation of genes regulated by RBP-J. Epstein-Barr virus nuclear antigen 2 (EBNA2) is essential for immortalization of human B cells by the virus. EBNA2 is a pleiotropic activator of viral and cellular genes and is targeted to DNA at least in part by interacting with RBP-J. We found that EBNA2 and the Notch1 RAMIC compete for binding to RBP-J, indicating that their interaction sites on RBP-J overlap at least partially. EBNA2 and Notch1 RAMIC transactivated the same set of viral and host promoters, i.e., the EBNA2 response element of the Epstein-Barr virus TP1 and the HES-1 promoter. Furthermore, EBNA2 functionally replaced the Notch1 RAMIC by suppressing differentiation of C2C12 myoblast progenitor cells

Topics: Virus-Cell Interactions
Publisher: American Society for Microbiology
Year: 1998
OAI identifier: oai:pubmedcentral.nih.gov:110408
Provided by: PubMed Central
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