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ID:39947078
大小:478.00 KB
页数:16页
时间:2019-07-15
《susceptibility of cem cell clones to gc-evoked apoptosiscem细胞克隆诱发细胞凋亡的gc敏感性》由会员上传分享,免费在线阅读,更多相关内容在教育资源-天天文库。
1、ROLEOFINTRACELLULARCALCIUMINGLUCOCORTICOID-EVOKEDLYMPHOIDCELLAPOPTOSISDevinMorrisCaliforniaStateUniversity,NorthridgeApoptosisReleaseofcyctochromecEffectorCaspasesApoptosisStimuli/DeathsignalsApoptosomeformationActivationofcaspasecascadeApaf-1Caspase9ProliferationCellPopulationCellDeathDevelopment
2、HomeostasisDiseasePhysiologicalrolesofapoptosisRIPCABCIPCRIPCRRRRRligandreceptorinteractingproteinscoactivatorcomplexbasaltrans.factors1234GlucocorticoidPathwaySusceptibilityofCEMCellClonestoGC-EvokedApoptosisGC-inducedIncreaseinIntracellularCalciuminGC-SusceptibleCEMcellsTime-&GC-Dose-DependentInc
3、reasein[Ca+2]iinCEM-C7-14CellsEtOH100nMDex1mMDex24hours48hours4.4%6%14.1%5%24.8%62.1%ABCDEFModulatorsof[Ca+2]iLevelsInfluenceGC-EvokedDeathofCEMCellsEGTASuppressesGC-EvokedIncreasein[Ca+2]iLevelsinCEM-C7-14CellsEtOH100nMDex1mMDexEthanol20mMEGTAABCDEF4.4%16.4%35%2%12.4%23.1%GlucocorticoidSignalingP
4、athwayPathwayInhibitorsNormalPathwayInhibitionofCalmodulinProtectsCEM-C7-14CellsfromGC-evokedDeathInhibitionofCalmodulinKinaseIIProtectsCEM-C7-14CellsfromGC-evokedDeathInhibitionofCalcineurinProtectsCEM-C7-14CellsfromGC-evokedDeathConclusionsGCsincrease[Ca+2]ilevelsonlyintheGC-susceptibleCEM-C7-14c
5、elllineinadosedependentmanner;notintheGC-resistantsistercellline,CEM-C1-15.CalciumchelationbyeitherBAPTAorEGTAprotectedCEM-C7-14cellsfromGC-evokedapoptosis,inconjunctionwithareductionintheamountoffree[Ca+2]i.ThecalciumionophoreA23187causessensitizationofCEM-C1-15cellstoGC-evokedapoptosis.Inhibition
6、ofcalmodulin,calmodulinkinaseIIorcalcineurin,allintermediatesinthecalciumsignalingpathway,impartvaryingdegreesofprotectiontoCEM-C7-14cellsfromGC-evokedapoptosis.OurdatademonstrateaclearcorrelationbetweencalciumsignalingandGC-evokedapoptosisFutureGoalsFurtherstudieswillaimtounderstandCa+2-dependentc
7、hangesingeneregulationthatcontributetoapoptosis.CandidategenessuchasthetranscriptionalrepressorE4BP4,anditsdownstreamtargetsarebeingstudied.OurultimategoalistounderstandthemolecularpathwayforapoptosisinT-ly
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