| Autor: |
Lee Yu K; National Research Laboratory of Molecular Virology, Department of Pathology, The Catholic University of Korea, Seoul 63071, Korea., Jung YM; National Research Laboratory of Molecular Virology, Department of Pathology, The Catholic University of Korea, Seoul 63071, Korea., Park SH; National Research Laboratory of Molecular Virology, Department of Pathology, The Catholic University of Korea, Seoul 63071, Korea., Lee SD; National Research Laboratory of Molecular Virology, Department of Pathology, The Catholic University of Korea, Seoul 63071, Korea., You JC; National Research Laboratory of Molecular Virology, Department of Pathology, The Catholic University of Korea, Seoul 63071, Korea. |
| Abstrakt: |
Gene expression in HIV-1 is regulated by the promoters in 5' long-terminal repeat (LTR) element, which contain multiple DNA regulatory elements that serve as binding sites for cellular transcription factors. YY1 could repress HIV-1 gene expression and latent infection. Here, however, we observed that virus production can be increased by YY1 over-expression and decreased under YY1 depleted condition by siRNA treatment. To identify functional domain(s) of YY1 activation, we constructed a number of YY1 truncated mutants. Our data show that full-length YY1 enhances the viral transcription both through U3 and U3RU5 promoters. Moreover, the C-terminal region (296-414 residues) of YY1 is responsible for the transcriptional upregulation, which could be enhanced further in the presence of the viral Tat protein. The central domain of YY1 (155-295 residues) does not affect LTR activity but has a negative effect on HIV-1 gene expression. Taken together, our study shows that YY1 could act as a transcriptional activator in HIV-1 replication, at least in the early stages of infection. [BMB Reports 2020; 53(5): 248-253]. |
