细胞程序化死亡总结.pptx

ProgrammedCellDeath;Apoptosis:shrink,havecondensednuclei,retainmembraneintegrity,rapidlyeliminatedbyphagocytosis.

Inapoptosis,Bcl2familyplaysapivotalroleinregulatingthereleaseofcytochromecandIAPantagonistsfrommitochondria.Theanti-apoptoticonesareBcl-2,Bcl-xl,Bcl-w,Mcl-1;andpro-apoptoticonesareBax,Bak,Bad,Bid,Bim.

Caspases,afamilyofcysteineproteases,areimportantinitiatorsandexecutorsinapoptosis.Theyareexpressedasinactivatedprecursors.Whileoncemeetingdeath-inducingstimuli,thespecificasparticresidueswillbecleavedandthesubunitsformtheactivatedprotease.Caspasefamilyisdividedtotwokinds-initiators(caspase8and9)andeffectors(caspase3,6,7).Apoptosomeprovidesaplatformforcaspase9cleavageandtheactivationofdeathreceptorwillleadtotheactivationofcaspase8.

;Figure1.EvolutionaryConservationoftheCoreApoptoticMachinery;autophagy;Dynamicsanddiversityinautophagymechanisms:lessonsfromyeast.HitoshiNakatogawa*?,KuninoriSuzuki*,YoshiakiKamada§andYoshinoriOhsumi*;Figure7|ModelfortheroleofconductorproteinsinPASorganization.Under

nutrient-richconditions,autophagy-related11(Atg11)servesasaconductor,together

withalargeassemblyofaminopeptidase1(Ape1;acargoprotein)andAtg19(a

receptor),torecruitotherAtgproteins,includingcoremachinerycomponentsandCvt

(cytoplasm-to-vacuoletargeting)-specificproteins.Thisrecruitmentorganizesthe

pre-autophagosomalstructure(PAS)tomediateCvtvesicleformationaroundthecargo

(leftpanel).AlthoughtheAtg17–Atg29–Atg31complex,whichisspecificallyrequiredfor

starvation-inducedautophagy,alsolocalizestothePASundertheseconditions,this

complexisdispensablefortheCvtpathway.Bycontrast,undernutrient-deprived

conditions,Atg17–Atg29–Atg31,togetherwithAtg1andAtg13,actsasaconductorina

mannerthatisindependentofAtg11.BythesemeansthePASisr