Functional replacement of the intracellular region of the Notch1 receptor by Epstein-Barr virus nuclear antigen 2
- PMID: 9621066
- PMCID: PMC110408
- DOI: 10.1128/JVI.72.7.6034-6039.1998
Functional replacement of the intracellular region of the Notch1 receptor by Epstein-Barr virus nuclear antigen 2
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.
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References
-
- Artavanis-Tsakonas S, Matsuno K, Fortini M E. Notch signaling. Science. 1995;268:225–232. - PubMed
-
- Aster J C, Robertson E S, Hasserjian R B, Turner J R, Kieff E, Sklar J. Oncogenic forms of NOTCH1 lacking either the primary binding site for RBP-Jκ or nuclear localization sequences retain the ability to associate with RBP-Jκ and activate transcription. J Biol Chem. 1997;272:11336–11343. - PubMed
-
- Ellisen L W, Bird J, West D C, Soreng A L, Reynolds T C, Smith S D, Sklar J. TAN-1, the human homolog of the Drosophila Notch gene, is broken by chromosomal translocations in T lymphoblastic neoplasms. Cell. 1991;66:649–661. - PubMed
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