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study reports that the DENV NS2B protease cofactor targets the DNA sensor cyclic GMP (show NT5C2 Proteins)-AMP (show APRT Proteins) synthase (cGAS) for lysosomal degradation to avoid the detection of mitochondrial DNA during infection.
This study demonstrates that the HCMV tegument protein pp65 (show LCP1 Proteins) inhibits IFN-beta (show IFNB1 Proteins) production by binding and inactivating cGAS early during infection. In addition, this inhibitory activity specifically targets cGAS, since it can be bypassed via the addition of exogenous cGAMP, even in the presence of pp65 (show LCP1 Proteins). Notably, STING proteasome-mediated degradation was observed in both the presence and absence of pp65 (show LCP1 Proteins).
TRIM56 (show TRIM56 Proteins) E3 ligase-induced monoubiquitination of cGAS is important for cytosolic DNA sensing and IFNalphabeta production to induce anti-DNA viral immunity.
Results indicate that the rs311678 polymorphism in the cyclic GMP (show NT5C2 Proteins)-AMP (show APRT Proteins) synthase (cGAS) gene confers genetic susceptibility to cervical precancerous lesions.
results suggest a nucleation-cooperativity-based mechanism for sensitive detection of mitochondrial DNA and pathogen genomes, and identify HMGB (show FAH Proteins)/TFAM (show TFAM Proteins) proteins as DNA-structuring host factors; they provide an explanation for the peculiar cGAS dimer structure and suggest that cGAS preferentially binds incomplete nucleoid-like structures or bent DNA
Study and report of the structure and catalytic mechanism of Cyclic GMP (show NT5C2 Proteins)-AMP (show APRT Proteins) synthase (cGAS).
Our results identify cGAS as mediator of an IFN-I response to HIV-1 infection in CD4 (show CD4 Proteins)(+) T cells and demonstrate that this response is modulated by the viral accessory proteins Vpr and Vpu. Thus, viral innate immune evasion is incomplete in the main target cells of HIV-1
miR (show MLXIP Proteins)-25/93 targets NCOA3 (show NCOA3 Proteins), an epigenetic factor that maintains basal levels of cGAS expression, leading to repression of cGAS during hypoxia. This allows hypoxic tumour cells to escape immunological responses induced by damage-associated molecular pattern molecules, specifically the release of mitochondrial DNA.
study identifies the AIM2 (show AIM2 Proteins) inflammasome and cGAS/IFI16 (show IFI16 Proteins)-STING-type I IFN pathway as a novel mechanism for host innate immunity to the ALVAC vaccine vector.
NEMO (show IKBKG Proteins) was critically involved in the cGAS-STING pathway.
Exhibits broad antiviral activity, most probably causing an early viral translation block.
chromosome 6 open reading frame 150
, cGAMP synthase
, cyclic GMP-AMP synthase
, mab-21 domain-containing protein 1
, protein MB21D1