Molecular mimicry of NF-κB by vaccinia virus protein enables selective inhibition of antiviral responses.
Ontology highlight
ABSTRACT: Infection of mammalian cells with viruses activates NF-κB to induce the expression of cytokines and chemokines and initiate an antiviral response. Here, we show that a vaccinia virus protein mimics the transactivation domain of the p65 subunit of NF-κB to inhibit selectively the expression of NF-κB-regulated genes. Using co-immunoprecipitation assays, we found that the vaccinia virus protein F14 associates with NF-κB co-activator CREB-binding protein (CBP) and disrupts the interaction between p65 and CBP. This abrogates CBP-mediated acetylation of p65, after which it reduces promoter recruitment of the transcriptional regulator BRD4 and diminishes stimulation of NF-κB-regulated genes CXCL10 and CCL2. Recruitment of BRD4 to the promoters of NFKBIA and CXCL8 remains unaffected by either F14
SUBMITTER: Albarnaz JD
PROVIDER: S-EPMC7614822 | biostudies-literature | 2022 Jan
REPOSITORIES: biostudies-literature
ACCESS DATA