| Autor: |
Sakai, Takashi, Taniguchi, Yoshihito, Tamura, Kumiko, Minoguchi, Shigeru, Fukuhara, Takataro, Strobl, Lothar J., Zimber-Strobl, Ursula, Bornkamm, George W., Honjo, Tasuku |
| Zdroj: |
The Journal of Virology; July 1998, Vol. 72 Issue: 7 p6034-6039, 6p |
| Abstrakt: |
ABSTRACTThe 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 TP1and the HES-1promoter. Furthermore, EBNA2 functionally replaced the Notch1 RAMIC by suppressing differentiation of C2C12 myoblast progenitor cells. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
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