Cellular RelB interacts with the transactivator Tat and enhance HIV-1 expression.
Cellular RelB interacts with the transactivator Tat and enhance HIV-1 expression.
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细胞 RelB 与反式激活因子 Tat 相互作用并增强 HIV-1 表达
DOI:
10.1186/s12977-018-0447-9
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发表时间:
2018-09-21
期刊:
影响因子:
3.3
通讯作者:
Qiao W
中科院分区:
文献类型:
--
作者:
Wang M;Yang W;Chen Y;Wang J;Tan J;Qiao W
BackgroundHuman immunodeficiency virus type 1 (HIV-1) Tat protein plays an essential role in HIV-1 gene transcription. Tat transactivates HIV-1 long terminal repeat (LTR)-directed gene expression through direct interactions with the transactivation-responsive region (TAR) element and otherciselements in the LTR. The TAR-independent Tat-mediated LTR transactivation is modulated by several host factors, but the mechanism is not fully understood.ResultsHere, we report that Tat interacts with the Rel homology domain of RelB through its core region. Furthermore, RelB significantly increases Tat-mediated transcription of the HIV-1 LTR and viral gene expression, which is independent of the TAR. Both Tat and RelB are recruited to the HIV-1 promoter, of which RelB facilitates the recruitment of Tat to the viral LTR. The NF-κB elements are key to the accumulation of Tat and RelB on the LTR. Knockout of RelB reduces the accumulation of RNA polymerase II on the LTR, and decreases HIV-1 gene transcription. Together, our data suggest that RelB contributes to HIV-1 transactivation.ConclusionsOur results demonstrate that RelB interacts with Tat and enhances TAR-independent activation of HIV-1 LTR promoter, which adds new insights into the multi-layered mechanisms of Tat in regulating the gene expression of HIV-1.
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DOI:
10.3390/v9040067
发表时间:
2017-04-01
期刊:
Viruses
影响因子:
--
作者:
Jean MJ;Power D;Kong W;Huang H;Santoso N;Zhu J
通讯作者:
Zhu J
影响因子:
3.3
作者:
Kim HY;Choi BS;Kim SS;Roh TY;Park J;Yoon CH
通讯作者:
Yoon CH
影响因子:
14.9
作者:
Dandekar, DH;Ganesh, KN;Mitra, D
通讯作者:
Mitra, D
DOI:
10.1073/pnas.0306764101
发表时间:
2004-03-23
影响因子:
11.1
作者:
Levy, DN;Aldrovandi, GM;Shaw, GM
通讯作者:
Shaw, GM
影响因子:
16
作者:
Barboric, M;Nissen, RM;Peterlin, BM
通讯作者:
Peterlin, BM