期刊
CELLS
卷 11, 期 18, 页码 -出版社
MDPI
DOI: 10.3390/cells11182812
关键词
cGAS; STING; calcium; autoimmunity; inflammation
类别
资金
- National Institutes of Health, USA [P01-HL 151327, HL-137179-01, HL-155941, HL-084153]
This review summarizes the regulatory mechanisms of cGAS activity, including structure, sub-cellular localization, post-translational modifications, and Ca2+ signaling. The role of cGAS activation in different diseases and clinical outcomes is also discussed.
Cyclic GMP-AMP synthase (cGAS) is a predominant and ubiquitously expressed cytosolic onfirmedDNA sensor that activates innate immune responses by producing a second messenger, cyclic GMP-AMP (cGAMP), and the stimulator of interferon genes (STING). cGAS contains a highly disordered N-terminus, which can sense genomic/chromatin DNA, while the C terminal of cGAS binds dsDNA liberated from various sources, including mitochondria, pathogens, and dead cells. Furthermore, cGAS cellular localization dictates its response to foreign versus self-DNA. Recent evidence has also highlighted the importance of dsDNA-induced post-translational modifications of cGAS in modulating inflammatory responses. This review summarizes and analyzes cGAS activity regulation based on structure, sub-cellular localization, post-translational mechanisms, and Ca2+ signaling. We also discussed the role of cGAS activation in different diseases and clinical outcomes.
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