TRIM14inhibitsOPTN-mediatedautophagic

degradationofKDM4Dtoepigeneticallyregulate

in?ammation

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)removesH3K4me3modi?-

multiplemechanisms.However,itremainsunclearhowautophagycationattheSocs1promotertoinhibittheexpressionof

epigeneticallyregulatestheimmuneresponse.Here,weidenti?edsuppressorofcytokinesignaling1(SOCS1),leadingtosignal

TRIM14asanepigeneticregulatorthatreduceshistoneH3K9tri-transducerandactivatoroftranscription4(STAT4)activation

methylati