Title | Guanylate Binding Protein 4 Negatively Regulates Virus-Induced Type I IFN and Antiviral Response by Targeting IFN Regulatory Factor 7 |
Authors | Hu, Yu Wang, Jie Yang, Bo Zheng, Nuoyan Qin, Meiling Ji, Yongyong Lin, Guomei Tian, Lin Wu, Xiaodong Wu, Li Sun, Bing |
Affiliation | Chinese Acad Sci, Lab Mol Cell Biol, Inst Biochem & Cell Biol, Shanghai Inst Biol Sci, Shanghai 200031, Peoples R China. Peking Univ, Tsinghua Univ, Joint Ctr Life Sci, Beijing 100084, Peoples R China. Tsinghua Univ, Sch Med, Beijing 100084, Peoples R China. Chinese Acad Sci, Mol Virus Unit, Key Lab Mol Virol & Immunol, Inst Pasteur Shanghai, Shanghai 200025, Peoples R China. Chinese Acad Sci, Lab Mol Cell Biol, Inst Biochem & Cell Biol, Shanghai Inst Biol Sci, 320 Yue Rd, Shanghai 200031, Peoples R China. |
Keywords | TOLL-LIKE RECEPTOR NF-KAPPA-B INTERFERON-ALPHA INDUCTION INNATE IMMUNITY RIG-I MEDIATED DEGRADATION PATHOGEN RECOGNITION INDUCIBLE GTPASES DENDRITIC CELLS RNA HELICASE |
Issue Date | 2011 |
Publisher | journal of immunology |
Citation | JOURNAL OF IMMUNOLOGY.2011,187,(12),6456-6462. |
Abstract | IRF7 is known as the master regulator in virus-triggered induction of type I IFNs (IFN-I). In this study, we identify GBP4 virus-induced protein interacting with IRF7 as a negative regulator for IFN-I response. Overexpression of GBP4 inhibits virus-triggered activation of IRF7-dependent signaling, but has no effect on NF-kappa B signaling, whereas the knockdown of GBP4 has opposite effects. Furthermore, the supernatant from Sendai virus-infected cells in which GBP4 have been silenced inhibits the replication of vesicular stomatitis virus more efficiently. Competitive coimmunoprecipitation experiments indicate that overexpression of GBP4 disrupts the interactions between TRAF6 and IRF7, resulting in impaired TRAF6-mediated IRF7 ubiquitination. Our results suggest that GBP4 is a negative regulator of virus-triggered IFN-I production, and it is identified as a novel protein targeting IRF7 and inhibiting its function. The Journal of Immunology, 2011, 187: 6456-6462. |
URI | http://hdl.handle.net/20.500.11897/394039 |
ISSN | 0022-1767 |
DOI | 10.4049/jimmunol.1003691 |
Indexed | SCI(E) |
Appears in Collections: | 生命科学学院 |