Application | Comment | Organism |
---|---|---|
medicine | cGAS activates the AKT and ERK pathways to promote the inflammatory response of rheumatoid arthritis fibroblast-like synoviocytes | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | Q8N884 | - |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
synoviocyte | rheumatoid arthritis synoviocyte | Homo sapiens | - |
General Information | Comment | Organism |
---|---|---|
physiological function | cGAS is overexpressed in rheumatoid arthritis fibroblast-like synoviocytes compared with osteoarthritis fibroblast-like synoviocytes. TNFalpha stimulation induces cGAS expression in rheumatoid arthritis fibroblast-like synoviocytes. Overexpression of cGAS promotes the proliferation and knockdown of cGAS inhibits the proliferation of rheumatoid arthritis fibroblast-like synoviocytes. cGAS overexpression enhances the production of proinflammatory cytokines and matrix metalloproteinases as well as AKT and ERK phosphorylation in TNFalpha-stimulated fibroblast-like synoviocytes. In contrast, cGAS silencing inhibits production of proinflammatory cytokines and matrix metalloproteinases as well as AKT and ERK phosphorylation in TNFalpha-stimulated fibroblast-like synoviocytes | Homo sapiens |