TRIM24 facilitates antiviral immunity through mediating K63-linked TRAF3 ubiquitination
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资源简介：
Ubiquitination is an essential mechanism in the control of antiviral immunity upon virus infection. Here, we identify a series of
ubiquitination-modulating enzymes that are modulated by vesicular stomatitis virus (VSV). Notably, TRIM24 is down-regulated
through direct transcriptional suppression induced by VSV-activated IRF3. Reducing or ablating TRIM24 compromises type I
IFN (IFN-I) induction upon RNA virus infection and thus renders mice more sensitive to VSV infection. Mechanistically, VSV
infection induces abundant TRIM24 translocation to mitochondria, where TRIM24 binds with TRAF3 and directly mediates K63-
linked TRAF3 ubiquitination at K429/K436. This modification of TRAF3 enables its association with MAVS and TBK1, which
consequently activates downstream antiviral signaling. Together, these findings establish TRIM24 as a critical positive
regulator in controlling the activation of antiviral signaling and describe a previously unknown mechanism of TRIM24 function.
提供机构：
中国科学院上海营养与健康研究所
创建时间：
2023-12-05
