| Literature DB >> 9621066 |
T Sakai1, Y Taniguchi, K Tamura, S Minoguchi, T Fukuhara, L J Strobl, U Zimber-Strobl, G W Bornkamm, T 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.Entities:
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Year: 1998 PMID: 9621066 PMCID: PMC110408
Source DB: PubMed Journal: J Virol ISSN: 0022-538X Impact factor: 5.103