EC Number   |
General Information |
Reference |
|---|
   2.7.7.86 | evolution |
beta2 and beta6 of cGAS harbor the signature catalytic site residues (E200, D202 and D296) of the NTase superfamily coordinating catalytic Mg2+ ions and nucleotides |
761268 |
| 2.7.7.86 | malfunction |
aberrant activation of cGAS is associated with various autoimmune disorders |
761723 |
| 2.7.7.86 | malfunction |
depletion of cGAS diminishes cGAS activity and decreases the expression of inflammatory genes while suppressing the upregulation of autophagy in Huntington disease (HD) cells, while reinstating cGAS in cGAS-depleted HD cells activates cGAS activity and promotes inflammatory and autophagy responses. Phenotype, overview |
-, 762288 |
| 2.7.7.86 | malfunction |
dysregulation of the cGAS pathway is linked to autoimmune diseases while targeted stimulation may be of benefit in immunoncology |
762338 |
| 2.7.7.86 | malfunction |
knockout or knockdown of the enzyme blocks cytokine induction by HIV, murine leukemia virus, and simian immunodeficiency virus. cGAS mutant cell lines fail to activate IRF3 in response to HT-DNA transfection or HSV-1 infection |
726489 |
| 2.7.7.86 | malfunction |
overexpression of chcGAS induces Ifn-beta and Il-1beta expression. ChcGAS-induced IFN-beta and IL-1beta expression is dependent on the STING signaling pathway. Ablation of chcGAS abrogates dsDNA-stimulated IFN-beta and IL-1beta expression. Knockdown of cGAS promotes FAdV-4 infection |
761268 |
| 2.7.7.86 | malfunction |
small molecule inhibition of cyclic GMP-AMP synthase by RU.521 ameliorates sepsis-induced cardiac dysfunction in mice. The inflammatory responses, oxidative stress and apoptosis in hearts of sepsis mice are markedly mitigated by RU.521. The septic mice that undergo RU.521 treatment exhibit suppressed myocardial apoptosis, which is indicated by decreased caspase-3 activity |
761781 |
| 2.7.7.86 | metabolism |
cellular intrinsic mechanism involving the cGAS-mediated cytosolic self-DNA-sensing pathway that initiates premature senescence independently of telomere shortening, overview. Micronuclei generated in response to telomeric DNA replication stress recruit cGAS and cause cellular senescence |
761514 |
| 2.7.7.86 | metabolism |
STING undergoes large conformational changes by binding to 2',3'-cGAMP and then recruits TANK binding kinase (TBK1), thus resulting in the phosphorylation of IFN-regulated factor 3 (IRF3) and nuclear factor-kappaB (NF-kappaB), and promoting the expression of IFNs and proinflammatory cytokines. chcGAS might be involved in sensing a DNA virus, FAdV-4, in LMH cells |
761268 |
| 2.7.7.86 | metabolism |
the relationship of cGAS and STING is both old (as much as much as 500 million years of co-evolution), and interesting in that cGAS is a low-activity enzyme while STING is a particularly avid binder of the cGAS product |
762338 |
