Zinc finger protein 64 promotes Toll-like receptor-triggered proinflammatory and type I interferon production in macrophages by enhancing p65 subunit activation.

ABSTRACT: The molecular mechanisms that fine-tune the Toll-like receptor (TLR)-triggered innate immune response need further investigation. As an important transcription factor, zinc finger proteins (ZFPs) play important roles in many cell functions, including development, differentiation, tumorigenesis, and functions of the immune system. However, the role of ZFP members in the innate immune responses remains unclear. Here we showed that the expression of C2H2-type ZFP, ZFP64, was significantly up-regulated in macrophages upon stimulation with TLR ligands, including LPS, CpG oligodeoxynucleotides, or poly(I:C). ZFP64 overexpression promoted TLR-triggered TNF-α, IL-6, and IFN-β production in macrophages. Coincidently, knockdown of ZFP64 expression significantly inhibited the production of the above

SUBMITTER: Wang C 

PROVIDER: S-EPMC3750158 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature