The TRIM14-USP14-BRCC3 complex epigenetically regulates inflammation through inhibiting OPTN-mediated autophagic degradation of KDM4D
The TRIM14-USP14-BRCC3 complex epigenetically regulates inflammation through inhibiting OPTN-mediated autophagic degradation of KDM4D
复制标题
TRIM14-USP14-BRCC3 复合物通过抑制 OPTN 介导的 KDM4D 自噬降解来表观遗传调节炎症
DOI：
10.1080/15548627.2022.2055286
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发表时间：
2022
期刊：
影响因子：
13.3
通讯作者：
Jun Cui
中科院分区：
文献类型：
--
作者：
Di Liu;Shouheng Jin;Jun Cui
摘要自噬是一种保守的真核生物过程，介导细胞器和蛋白质聚集体的降解，参与多种细胞反应，包括免疫信号转导。KDM 4D是一种重要的组蛋白去甲基化酶，通过抑制组蛋白H3 K9的三甲基化来调节基因的转录。自噬是否通过调节KDM 4D的稳定性和活性在表观遗传学上调节免疫反应仍不清楚。最近，我们确定TRIM 14（tripartary motif-containing 14）为表观遗传调节因子，其招募USP 14和BRCC 3形成调节复合物，并通过抑制OPTN介导的KDM 4D自噬降解来促进炎症反应。
ABSTRACT Macroautophagy/autophagy is a conserved eukaryotic process to mediate the degradation of cell organelles and protein aggregates, which participates in a variety of cellular responses, including immune signal transduction. KDM4D functions as an important histone demethylase to regulate gene transcription by inhibiting histone H3K9 trimethylation. Whether autophagy epigenetically regulates the immune response via modulating the stability and activity of KDM4D remains largely unclear. Recently, we identified TRIM14 (tripartite motif-containing 14) as an epigenetic regulator, which recruits USP14 and BRCC3 to form a regulatory complex, and promotes an inflammation response through inhibiting OPTN-mediated autophagic degradation of KDM4D.