| Autor: |
Reddy, Thipparthi R., Xu, Weidong, Mau, Jonathan K. L., Goodwin, Christopher D., Suhasini, Modem, Tang, Hengli, Frimpong, Kenneth, Rose, David W., Wong-Staal, Flossie |
| Předmět: |
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| Zdroj: |
Nature Medicine; Jun1999, Vol. 5 Issue 6, p635, 8p |
| Abstrakt: |
The HIV-1 Rev protein facilitates the nuclear export of mRNA containing the Rev response element (RRE) through binding to the export receptor CRM-1. Here we show that a cellular nuclear protein, Sam68 (Src-associated protein in mitosis), specifically interacts with RRE and can partially substitute for as well as synergize with Rev in RRE-mediated gene expression and virus replication. Differential sensitivity to leptomycin B, an inhibitor of CRM-1, indicates that the export pathways mediated by Rev and Sam68 are distinct. C-terminally deleted mutants of Sam68 inhibited the transactivation of RRE-mediated expression by both wild-type Sam68 and Rev. They were retained in the cytoplasm and impeded the nuclear localization of Rev in coexpressed cells. These mutants also inhibited wild-type HIV-1 replication to the same extent as the RevM10 mutant, and may be useful as anti-viral agents in the treatment of AIDS. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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