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TRIM14 inhibits OPTN-mediated autophagic degradation of KDM4D to epigenetically regulate inflammation
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TRIM14 inhibits OPTN-mediated autophagic degradation of KDM4D to epigenetically regulate inflammation
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Journal Article
TRIM14 inhibits OPTN-mediated autophagic degradation of KDM4D to epigenetically regulate inflammation
2022
Overview
Autophagy is a fundamental cellular process of protein degradation and recycling that regulates immune signaling pathways via multiple mechanisms. However, it remains unclear how autophagy epigenetically regulates the immune response. Here, we identified TRIM14 as an epigenetic regulator that reduces histone H3K9 trimethylation by inhibiting the autophagic degradation of the histone demethylase KDM4D. TRIM14 recruited the deubiquitinases USP14 and BRCC3 to cleave the K63-linked ubiquitin chains of KDM4D, which prevented KDM4D from undergoing optineurin (OPTN)-mediated selective autophagy. Tripartite motif-containing 14 (TRIM14) deficiency in dendritic cells significantly impaired the expression of the KDM4D-directed proinflammatory cytokines interleukin 12 (Il12) and Il23 and protected mice from autoimmune inflammation. Taken together, these findings highlight the cross-talk between epigenetic regulation and autophagy and suggest TRIM14 is a potential target of therapeutic intervention for inflammation-related diseases.
Publisher
National Academy of Sciences
Subject
/ Cell Cycle Proteins - genetics
/ Cell Cycle Proteins - metabolism
/ Encephalomyelitis, Autoimmune, Experimental - genetics
/ Encephalomyelitis, Autoimmune, Experimental - metabolism
/ Female
/ Histones
/ Intracellular Signaling Peptides and Proteins - genetics
/ Intracellular Signaling Peptides and Proteins - metabolism
/ Jumonji Domain-Containing Histone Demethylases - genetics
/ Jumonji Domain-Containing Histone Demethylases - metabolism
/ Membrane Transport Proteins - genetics
/ Membrane Transport Proteins - metabolism
/ Mice
/ Specific Pathogen-Free Organisms
/ Tripartite Motif Proteins - genetics
