Identification and characterization of MAVS, a mitochondrial antiviral signaling protein that activates NF-kappaB and IRF 3.
By Rashu B. Seth, Lijun Sun, Chee-Kwee Ea, Zhijian J. Chen. Cell, 2005
1,897 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/d1088cc9e4c936b7f33dbf165f316ce45dda197b
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- Lijun Sun
- Yasuo Tanaka
- Xin Cai
- Y. Chiu
- Siqi Liu
- Zhijian J. Chen
- D. Kolakofsky
- F. Hou
Citations in the corpus
- The specific and essential role of MAVS in antiviral innate immune responses. (2006, methodology): “The adaptor protein that links RIG-I to IKK and TBK1/ IKK3 activation is the recently identified MAVS (Seth et al., 2005), also known as IPS-1 (Kawai et al., 2005), VISA (Xu et al., 2005), or CARDIF (Meylan et al., 2005).”
- Phosphorylation of innate immune adaptor proteins MAVS, STING, and TRIF induces IRF3 activation (2015, methodology): “The rabbit antibodies against human MAVS and STING were generated as described before (24, 35).”
- RNA polymerase III detects cytosolic DNA and induces type I interferons through the RIG-I pathway. (2009, background): “Although the DNA-binding protein DAI (ZBP1) has been proposed as a DNA sensor that induces type I IFNs, DAI-deficient mice and cells from these mice do not have apparent defects in producing type I IFNs in response to DNA stimulation (Ishii et al., 2008; Takaoka et al., 2007).”
- Cyclic GMP-AMP Containing Mixed Phosphodiester Linkages Is An Endogenous High Affinity Ligand for STING (2013, unknown): “MAVS, an essential adaptor protein of the RIG-I pathway (Seth et al., 2005), was able to induce IFNb in all of these cell lines.”
- Type I interferon inhibits interleukin-1 production and inflammasome activation. (2011, background): “This gives rise to anefficient interaction with MAVS/VISA/IPS-1/Cardif, a crucial downstream adaptor protein (Kawai et al., 2005; Meylan et al., 2005; Seth et al., 2005; Xu et al., 2005), leading to the recruitment of signaling molecules such as the TBK1 complex to MAVS.”