EC Number |
Natural Substrates |
---|
3.4.21.98 | CARDIF + H2O |
NS3-4A cleaves Cardif (adaptor protein of retinoic acid-inducible gene I or melanoma differentiation-associated gene-5), resulting in an interruption of the Cardif-mediated pathway in non-neoplastic human hepatocyte PH5CH8 cells |
3.4.21.98 | CARDIF + H2O |
NS3-4A cleaves Cardif (CARD adaptor-inducing) by generating a 70 kDa fragment. NS3-4A-mediated cleavage, is not caspase-dependent. Cardif mutant C508A is resistant to NS3-4A-mediated cleavage |
3.4.21.98 | caspase recruitment domain adaptor-inducing IFN-beta (Cardif) + H2O |
- |
3.4.21.98 | hepatitis C virus polyprotein + H2O |
mutational cleavage |
3.4.21.98 | hepatitis C virus polyprotein + H2O |
the enzyme is essential for processing of viral polyprotein |
3.4.21.98 | hepatitis virus C polyprotein + H2O |
maturation of the viral polyprotein |
3.4.21.98 | mitochondrial antiviral signaling protein + H2O |
i.e. MAVS, cleavage at Cys-508 |
3.4.21.98 | more |
NS3-4A lacks the ability to cleave endogenous TRIF, regardless of HCV strains derived from patients with different stages of hepatic disease. Inflammatory cytokine production by NF-kappaB activation via the TRIF-mediated pathway also remains unsuppressed by NS3-4A |
3.4.21.98 | more |
NS3/4A protease is responsible for cleaving the viral polyprotein at junctions 3-4A, 4A4B, 4B5A, and 5A5B and two host cell adaptor proteins of the innate immune response, TRIF and MAVS |