MAVS and viral infectious disease: Besides, Arimoto et al. have noted that RNF125 mediates the K48-linked ubiquitination and subsequent degradation of RIG-I via proteasomes and directly interacts with MDA5 and MAVS to suppress MDA5- as well as MAVS- mediated signaling in a Ub conjugation-dependent manner, thereby dramatically repressing IFN-I production to potentiate viral infection.214 In addition, after IFN-I or poly(I:C) treatment, the RNF125 production is upregulated, inhibiting RIG-I-mediated IFN-I responses in a negative-feedback manner.