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TRIM14inhibitsOPTN-mediatedautophagic
degradationofKDM4Dtoepigeneticallyregulate
inflammation
a,1a,b,1a,1aaaa,2
DiLiu,ZhiyaoZhao,YuanchuShe,LeiZhang,XiangtianChen,LingMa,andJunCui
aGuangdongProvinceKeyLaboratoryofPharmaceuticalFunctionalGenes,MOEKeyLaboratoryofGeneFunctionandRegulation,StateKeyLaboratoryof
Biocontrol,SchoolofLifeSciences,SunYat-senUniversity,Guangdong510275,People’sRepublicofChina;andbDepartmentofInternalMedicine,Guangzhou
InstituteofPediatrics,GuangzhouWomenandChildren’sMedicalCenter,Guangdong510623,People’sRepublicofChina
EditedbyNoboruMizushima,DepartmentofBiochemistryandMolecularBiology,UniversityofTokyo,GraduateSchoolandFacultyofMedicine,Tokyo,
Japan;receivedJuly21,2021;acceptedJanuary5,2022byEditorialBoardMemberTadatsuguTaniguchi
Autophagyisafundamentalcellularprocessofproteindegrada-membranebindingofCD14toprimarymacrophages(16).
tionandrecyclingthatregulatesimmunesignalingpathwaysviaLysinedemethylase5A(KDM5A)removesH3K4me3modifi-
multiplemechanisms.However,itremainsunclearhowautophagycationattheSocs1promotertoinhibittheexpressionof
epigeneticallyregulatestheimmuneresponse.Here,weidentifiedsuppressorofcytokinesignaling1(SOCS1),leadingtosignal
TRIM14asanepigeneticregulatorthatreduceshistoneH3K9tri-transducerandactivatoroftranscription4(STAT4)activation
methylati
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