Mitochondriaparticipateinapoptoticsignalingpathwaysthroughthereleaseofmitochondrialproteinsintothecytoplasm.Cytochromec,akeyproteininelectrontransport,isreleasedfrommitochondriainresponsetoapoptoticsignals,andactivatesApaf-1,aproteasereleasedfrommitochondria.ActivatedApaf-1activatescaspase-9andtherestofthecaspasepathway.Smac/DIABLOisreleasedfrommitochondriaandinhibitsIAPproteinsthatnormallyinteractwithcaspase-9toinhibitapoptosis.ApoptosisregulationbyBcl-2familyproteinsoccursasfamilymembersformcomplexesthatenterthemitochondrialmembrane,regulatingthereleaseofcytochromecandotherproteins.TNFfamilyreceptorthatcauseapoptosisdirectlyactivatethecaspasecascade,butcanalsoactivateBid,aBcl-2familymember,whichactivatesmitochondria-mediatedapoptosis.Bax,anotherBcl-2familymember,isactivatedbythispathwaytolocalizetothemitochondrialmembraneandincreaseitspermeABIlity,releasingcytochrecandothermitochondrialproteins.Bcl-2andBcl-xLpreventporeformation,blockingapoptosis.AIF(Apoptosisinducingfactor)isanothermitochondrialfactorthatisreleasedintothecytoplasmtoinduceapoptosis.AIF-inducedapoptosisisimportantduringdevelopmentbutisnotcaspasedependent.

Contributor:GlennCroston,PhD

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