| Autor: |
Gong, Jian, Shen, Xi-Hui, Qiu, Hui, Chen, Chao, Yang, Rong-Ge |
| Předmět: |
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| Zdroj: |
Archives of Virology; Nov2011, Vol. 156 Issue 11, p1997-2006, 10p |
| Abstrakt: |
TRIM5α has been identified as the main restriction factor responsible for resistance of Old World monkey cells to HIV-1 infection. The precise mechanism of viral inhibition by TRIM5α remains elusive but appears to occur in multiple ways. Here, we report that rhesus monkey TRIM5α (TRIM5α) can represses HIV-1 LTR promoter activity by negatively regulating TAK1/TAB1/TAB2/TAB3-complex-mediated NF-κB activation when TRIM5α is overexpressed. We show that the overexpressed TRIM5α can interact with the TAK1/TAB1/TAB2/TAB3 complex by binding to TAB1 and promotes the degradation of TAB2 within the complex via the lysosomal degradation pathway. Subsequently, TRIM5α lowers the IKKα protein level and inhibits NF-κB p65 phosphorylation, and knockdown of TRIM5α expression by small interfering RNA in TRIM5α-overexpressing cells can abolish this inhibition. Finally, the inhibition of p65 phosphorylation results in the repression of HIV-1 LTR promoter activity. Taken together, these findings indicate that TRIM5α plays a previously unrecognized role in repressing HIV-1 transcription by inhibiting TAK1/TAB1/TAB2/TAB3-complex-mediated NF-κB activation when TRIM5α is overexpressed. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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