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SETD3介导的NF-κB抑制因子（NFKBIB）甲基化可调控病毒感染期间NF-κB介导的干扰素激活反应
NFKBIB methylation by SETD3 controls NF-κB-mediated interferon activation during viral infection
Ruiqi Sun, Boxuan Yin, Lilin Zhang, Yanyu Guo, Changyan Li, Yuchao Yan, Xinyi Zhang, Junyang Zhang, Zexing Li, Jinhai Huang
Journal：FEBS Journal
IF：4.2
DOI：10.1111/febs.70743
PMID：42799327
Published：2026-09-26
research field：毒理学伤口护理药剂学生物医学工程呼吸生物学材料科学
Abstract
The activation and regulation of type I interferon (IFN-I) is essential for the antiviral response and while epigenetic modifiers are known for regulating cellular signaling and responses by modifying nonhistone substrates, their role in IFN-I signaling remains uncertain. Here, through high-throughput screening, we identified the methyltransferase SETD3 as a positive regulator of IFN-I signaling. Specifically, deficiency of SETD3 markedly compromised the innate immune response to various stimuli. Mechanistically, SETD3 mediates NFKBIB methylation on lysine 235 which reinforces the binding of NFKBIB to P62. This promotes the autophagic degradation of NFKBIB and the subsequent release and nuclear translocation of NF-κB, ultimately regulating the transcription of downstream genes. Thus, we reveal the critical role of SETD3-mediated NFKBIB methylation in enhancing IFN-I signaling, highlighting the potential of SETD3 in controlling viral infections.
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