Effect of RelB on HIV-1 Vpr-mediated transcription activation and cell G2/M arrest.
- Author:
Rui-Kang LIU
1
;
Yang GAO
;
Yong-Quan LIN
;
Juan TAN
;
Yun-Qi GENG
;
Wen-Tao QIAO
Author Information
1. Key Laboratory of Molecular Microbiology and Biotechnology, Ministry of Education, College of Life Sciences, Nankai University, Tianjin 300071, China.
- Publication Type:Journal Article
- MeSH:
Cell Cycle Checkpoints;
Cell Division;
G2 Phase;
HIV Long Terminal Repeat;
HeLa Cells;
Humans;
NF-kappa B;
genetics;
Transcription Factor RelB;
physiology;
Transcriptional Activation;
vpr Gene Products, Human Immunodeficiency Virus;
physiology
- From:
Chinese Journal of Virology
2013;29(1):44-50
- CountryChina
- Language:Chinese
-
Abstract:
Vpr, an auxiliary protein of HIV-1(Human immunodeficiency virus type 1), exerts important functions to promote viral replication and AIDS progression. In this study, we performed a yeast two-hybrid screening assay using human cDNA library to further investigate the molecular mechanism of various functions of Vpr RelB, a key protein in NF-kappaB signaling pathway, was identified as a Vpr interaction protein by co-immunoprecipitation. Further investigations indicated that RelB not only promoted the Vpr-mediated activation of NF-kappaB reporter gene, but also enhanced the transactivation of HIV LTR. Moreover, the results showed that RelB promoted Vpr-induced cell cycle G2/M arrest. Collectively, these results indicated that RelB might interact with Vpr and regulate its transcriptional activation and cell cycle arrest.
