The Ca²⁺-dependent phosphatase calcineurin dephosphorylates TBK1 to suppress antiviral innate immunity.

ABSTRACT: Tumor necrosis factor receptor-associated factor family member-associated NF-κB activator-binding kinase 1 (TBK1) plays a key role in the induction of the type 1 interferon (IFN-I) response, which is an important component of innate antiviral defense. Viruses target calcium (Ca²⁺) signaling networks, which participate in the regulation of the viral life cycle, as well as mediate the host antiviral response. Although many studies have focused on the role of Ca²⁺ signaling in the regulation of IFN-I, the relationship between Ca²⁺ and TBK1 in different infection models requires further elucidation. Here, we examined the effects of the Newcastle disease virus (NDV)-induced increase in intracellular Ca²⁺ levels on the suppression of host antiviral res

SUBMITTER: Qu Y 

PROVIDER: S-EPMC11092360 | biostudies-literature | 2024 May

REPOSITORIES: biostudies-literature