简介：Weisolatedandpurifiedmitochondriafrommouseliversandspinachleaves.WhenaddedintoeggextractsofXenopuslaevis,theycausednucleiofmouselivertoundergoapoptoticchanges.Chromatincondensation,marginationandDNAladderwereobserved.Afterincubatingisolatedmitochondriainsomehypotonicsolutions,andcentrifugingthesemixturesatmghspeed,wegotmitochondrialsupernatants.Itwasfoundthatintheabsenceofcytosolicfactor,thesupernatantalonewasabletoinduceapoptoticchangesinnuclei.Theeffectivecomponentswerepartlyofprotein.DNAfragmentationwaspartlyinhibitedbycaspaseinhibitorsAC-DEVD-CHOandAC-YVAD-CHO.Meanwhile,caspaseinhibitorsfullyblockedchromatincondensation.Primarycharacterizationofthenuclearendonuclease(s)inducedbymitochondrialsupernatantswasalsoconducted.ItwasfoundthatthisendonucleaseisdifferentfromendonucleaseG,cytochromec-inducednuclease,orCa^2+-activatedendonuclease.

简介：Stressinducedtheseriousdisorderofcardiacfunctionandcardiovasculardiseases.Apoptosisisthecellularbasisinstressinducedcardiacinjury.Inourpreviousstudywefoundthatmanystressorsresultedinmitochondrialdamage.Itiscertainthatmitochondriaisimportantmediatorintriggeringapoptoticcelldeath,butthemechanism,bywhichthestressinducedmitochondrialinjuryleadstocardiomyocyteapoptosis,remainsunclear.Wedesignedthepresentstudytoinvestigatethechangesofthemitochondriaincardiomyocytesundergoingstressanditsroleininducingapoptosis.Herewereportedthatstresschangedthemembranefluidityofmitochondriaandinducedthelipidperoxidationofmitochondrialmembranein

简介：Uponencounteringtheantigen(Ag),theimmunesystemcaneitherdevelopaspecificimmuneresponseofenteraspecificstateofunresponsiveness,tolerance.TheresponseofBcellstotheirspecificAgcanbeactivationandproliferation,leadingtotheimmuneresponse,oranergyandactivation-inducedcelldeath(AICD),leadingtotolerance.AICDinBlymphocytesisahighlyregulatedeventinitiatedbycrosslinkingoftheBcellreceptor(BCR).BCRengagementinitiatesseveralsignalingeventssuchasactivationofPLCγ,Ras,andPI3K,whichgenerallyspeaking,leadtosurvival.However,intheabsenceofsurvivalsignals(CD40orIL-4Rengagement),BCRcrosslinkingcanalsopromoteapoptoticsignaltransductionpathwayssuchasactivationofeffectorcaspases,expressionofpro-apoptoticgenes,andinhibitionofpro-survivalgenes.ThecomplexinterplaybetweensurvivalanddeathsignalsdeterminestheBcellfateand,consequently,theimmuneresponse.

简介：Anuranmetamorphosisinvolvessystematictransformationsofindividualorgansinathyroidhormone(TH)-dependentmanner.Morphologicalandcellularstudieshaveshownthattheremovaloflarvalorgans/tissuessuchthetailandthetadpoleintestinalepitheliumisthroughprogrammedcelldeathorapop-tosis.RecentmolecularinvestigationssuggestthatTHregulatesmetamorphosisbyregulatingtargetgeneexpressionthroughthyroidhormonereceptors(TRs),whichareDNA-bindingtranscriptionfactors.Cloning

简介：在不到10年里自从它的开始，RNA干扰(RNAi)在生物医学的科学上有非凡的影响。RNAi被表明了到影响众多生物并且疾病小径。RNAi技术的开发和采纳是丰富的从基本loss-of-function工具，到药品的目标确认的染色体宽的屏蔽图书馆和治疗学的开发。然而，RNAiis的分子的机制理解远非完全。这简短评论的目的是在阐明加亮关键成就导致RNA的silencing建筑群并且到的生化学机制为这块地构画出主要挑战。

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简介：到米饭异种的分子的水平上的变化的特征在空间环境导致了的进一步的学习，我们在四米饭异种(二high-tillering和二low-tillering)的叶子和种子分析了蛋白质在8(th)并且9(th)在一架15天的空间班机以后的代，并且与他们由two-dimentionalpolyacrylamide的扎根的控制相比，凝胶电泳和颠倒分阶段执行液体层析(RPLC)。另外，变异的种子的白朊，血球素，谷醇溶蛋白，谷蛋白，和直链淀粉被RPLC和紫外线spectrometry分析。结果证明在山峰的叶子的低丰富的蛋白质是到ering舞台为止更可能的与他们的相应控制相比被导致。当时，揭示的变异的种子的白朊，血球素，和谷醇溶蛋白变化稳定地与他们在不同异种的变化的控制，和特征相比被继承在8(th)并且9(th)代，建议他们能被用作简历标记到异种由空间飞行导致了的身份。而且，二蛋白质(SSP9111和SSP6302)被发现在不同异种与高紧张(双重的变化)被表示，它两个都根据集体spectrometry并且数据库寻找与相片系统被相关。

简介：植物荷尔蒙植物生长素在调整植物生长和开发起一个关键作用。最近的进展在植物生长素反应小径的理解被做了，首先由在Arabidopsis的植物生长素反应异种的描述。另外，microRNAs(miRNAs)被显示了是为正常植物开发和生理学重要的基因的批评管理者。然而，很少对在miRNAs并且在正常开发期间的神经质的发信号之间的可能的相互作用被知道。这里，我们显示出那ArabidopsismicroRNA，miR167，有一个互补序列到AUXIN反应FACTOR6(ARF6)和ARF8mRNAs的部分，能为ARF8，然而并非为ARF6引起抄本降级。我们报导35S::MIR167b的phenotypic描述转基因的线，和表演转基因的线有的那严重35S::MIR167barf6arf8的类似于那些的显型加倍异种。转基因的显型建议miR167可以镇压在翻译的水平的ARF6。我们证明转基因的植物在花的机关的所有四锭盘是有缺点的。在转基因的花，细丝是反常地短的，花药不能适当地释放花粉，并且花粉谷物没发芽。我们的结果提供在表明网络支持的基因表示和植物生长素的调停miRNA的规章的小径之间的一个重要连接种繁殖开发。

简介：HELcells,ahumanerythroleukemiacellline,mainlyexpressthefetal(γ)globingeneandtraceamountoftheembryonic(ε)globingene,butnotadult(β)globingene.Hereweshowthathydroxyurea(HU)caninduceHELcellstoexpressadult(β)globingeneandleadthesecellstoterminaldifferentiation.ResultsshowedinGelmobilityshiftassaysthatGATAfactorscouldspecificallybindtotheregulatoryelementsofhumanβ-globingene,includingtheproximalregulatoryelement(theβ-promoter)andthedistalregulatoryelements(theDNaseIhypersensitivesitesintheLCR,HS2-HS4coresequences).However,theDNAbindingpatternsofGATAfactorswerequitedifferentbetweenHU-inducedanduninducedHELcells.Western-blotanalysisofnuclearextractsfromboththeuninducedandHU-inducedHELcellsrevealedthatthelevelofGATA-2transcriptionfactordecreased,whereasthelevelofGATA-1transcriptionfactorincreasedfollowingthetimeofhydroxyureainduction.Furthermore,usingRT-PCRanalysistheexpressionofhumanβ-globingeneinHU-inducedHELcellscouldbeblockedagainwhenHELcellswereincubatedinthepresenceofantisenseoligonucleotidesforhGATA-1,suggestingthattheupregulationofhGATA-1transcriptionfactormightbecriticalfortheexpressionofhumanβ-globingeneinHU-inducedHELcells.

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简介：Oneofmanyinterestingresearchactivitiesinbiofluidmechanicsisdedicatedtoinvestigationsoflocomotioninwater.Someofpropulsionmechanismsobservedintheunderwaterworldareusedinthedevelopmentprocessofunderwaterauto-nomicvehicles(AUV).Inordertocharacteriseseveralsolutionsaccordingtotheirmanoeuvrability,influenceonthesur-roundingfluidandenergeticefficiency,adetailedanalysisoffin-likemovementisindispensable.Inthecurrentpaperananalysisofundulatory,oscillatoryandcombinedfin-likemovementsbymeansofnumericalsimulationiscarriedout.TheconservationequationofmassandtheconservationequationofmomentumaresolvedwiththeFiniteVolumeMethod(FVM)byuseofthesoftwareCFX-10.0.Theundulatoryandoscillatoryfinmovementsaremodelledwithanequationthatisimplementedwithinanadditionalsubroutineandjoinedwiththemainsolver.Numericalsimulationsarecarriedoutinthecomputationaldomain,inwhichonefinisfixedinaflow-throughwaterduct.SimulationsarecarriedoutintherangeoftheRenumberupto105.Theresultsshowsignificantinfluenceofappliedfinmotiononthevelocitydistributioninthesurroundingfluid.

简介：人的免疫不全病毒类型1(HIV-1)Vpr导致房间死亡在哺乳动物并且分裂酵母房间，建议那Vpr可以影响一个保存细胞的过程。然而，导致Vpr的酵母房间死亡是否在哺乳动物的房间模仿调停Vpr的apoptosis，是不清楚的。我们最近识别了很多Vprsuppressors不仅在分裂酵母压制导致Vpr的房间死亡，而且在哺乳动物的房间堵住导致Vpr的apoptosis。这些调查结果建议在酵母的导致Vpr的房间死亡可以类似于一些哺乳动物的房间的apoptotic过程。这研究的目标是为apoptosis的未来研究开发并且验证一个分裂酵母模型系统。类似于在哺乳动物的房间的导致Vpr的apoptosis，我们这里证明在分裂酵母的Vpr支持phosphatidylserine外表表现并且导致线粒体的hyperpolarization，导致mitochondrial膜潜力的变化。而且，反应的氧种类(ROS)的Vpr扳机生产，显示象apoptotic一样细胞死亡可能被ROS调停。有趣地，Vpr在可以为在分裂酵母测量象apoptotic一样过程提供一个简单标记的线粒体导致唯一的词法变化。验证这可能性，我们测试了二Vprsuppressors(EF2和Hsp16)除了最新识别的Vprsuppressor(Skp1)在哺乳动物的房间压制导致Vpr的apoptosis。所有三蛋白质废除了房间死亡由Vpr调停了并且在酵母房间恢复了正常mitochondrial形态学。在结论，在分裂酵母的导致Vpr的房间死亡类似于哺乳动物的apoptotic过程。分裂酵母可以潜在地因此为Vpr和另外的proapoptotic代理人导致的象apoptotic一样过程的未来学习被用作一个简单模型有机体。

简介：

简介：Formationofapoptoticbodiesisatypicalcharacterofapoptoticcelldeath,buthowtheprocessesarecontrolledisnotknown.Inthisstudy,wecomparedtwoapoptosisinducingsystemsinvascularendothelialcells(VEC).Wefoundthattheformationofapoptoticbodiesduringapoptosisinducedbyrattlesnakevenom,whichisanuniqueandspecificapoptosisinducertovascularendothelialcells,wasmuchfasterthanthatinducedbydeprivationofsurvivalfactors(aFGFandserum).WhenweblockedthesynthesisofmRNAsincellstreatedwithrattlesnakevenombyDRB(5,6-dichloro-1-β-D-ribofuranosylbenzimidazole),aninhibitoroftranscription,theformationofapoptoticbodieswasdramaticallyinhibited.WeexaminedtheexpressionofP^53geneandfoundthatitsexpressionwasmuchhigherinapoptosisinducedbyrattlesnakevenomthatthatinapoptosisinducedbydeprivationofaFGFandserum.OurresultssuggestthatgeneexpressionisimportantandP^53genemayplayamajorroleininducingtheformationofapoptoticbodiesinVEC.

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简介：肿瘤坏死因素(TNF)联系了导致apoptosisligand(TRAIL/APO2L)是在血缘的死亡受体的约会之上导致apoptosis的TNF基因总科的一个成员。当小道对正常房间相对无毒时，它有选择地在许多转变房间导致apoptosis。不过，胸肿瘤房间对小道的效果特别地抵抗。这里，我们报导在有cyclin依赖的kinase禁止者roscovitine的联合，落后于的暴露在检验的小道抵抗的乳癌房间线的多数导致了显著apoptosis。Roscovitine便于小道导致死亡的发信号的复杂形成和caspase-8的激活。FLICE禁止的蛋白质是的cFLIP(L)和cFLIP显著地下面调整的列在后面暴露到roscovitine并且，确实由siRNA的cFLIPisoforms击倒敏化的胸肿瘤房间到导致小道的apoptosis。另外，我们证明roscovitine强烈在胸肿瘤房间压制了Mcl-1表示和起来调整的E2F1蛋白质层次。显著地，由siRNA的Mcl-1的silencing敏化胸肿瘤房间到导致小道的apoptosis。而且，由减少的siRNA的E2F1蛋白质击倒在导致小道的apoptosis的roscovitine的敏化的效果。在摘要，我们的结果为roscovitine的pro-apoptotic影响揭示pleitropic机制，加亮它象在在有小道的联合的乳癌的一个反肿瘤代理人的潜力。

简介：人的导致的pluripotent茎(iPS)房间类似于胚胎的茎(ES)房间，和罐头强烈地增殖并且区分进许多房间类型。然而，人的iPS房间的肝的区别还没被报导了。在这份报告，人的iPS房间被导致由一个逐步的协议区分进肝的房间。肝房间标记的表达式和人的iPS的肝相关的函数导出房间的房间被监视并且与区分的人的ES房间和主要人的hepatocytes的相比。在白天7点的约60%区分的人的iPS房间表示了肝的标记alphafetoprotein和白长袍的。在白天21点的区分的房间包括白朊Asecretion，肝糖合成，脲生产和可诱导的细胞色素P450活动展出了肝房间功能。肝的标记的表示和iPS的肝相关的功能导出房间的肝的房间比得上人的ES导出房间的肝的房间的。这些结果证明人的iPS房间，类似于人的ES房间，能高效地被导致区分房间进象hepatocyte一样。

简介：CellsregulatephospholipaseD(PLD)activityinresponsetonumerousextracellularsignals.Here,weinvestigatedtheinvolvementofPLDactivityintransforminggrowthfactor-β(TGF-β1)-mediatedgrowthinhibitionofepithelialcells.TGF-β1)-mediatedgrowthinhibitionofepithelialcells.TGF-β1inhibitsthegrowthofMDCK,Mv1Lu,andA-549cells.Inthepresenceof0.4%butanol,TGF-β1inducesanincreaseintheformationofphosphatidylbutanol,auniqueproductcatalyzedbyPLD.TGF-β1alsoinducesanincreaseinphosphatidicacid(PA)levelinA-549andMDCKcells.TGF-β1inducesanincreaseinthelevelsofDAGlabeledwith[^3H]-myristicacidinA-549andMDCKcellsbutnotinMv1Lucells.NoincreaseofDAGwasobservedincellsprelabeledwith[^3H]-arachidonicacid.ThedatapresentedsuggestthatPLDactivationisinvolvedintheTGF-β1-inducedcellgrowthinhibition.

简介：Theeventsofcelldeathandtheexpressionofnuclearmatrixprotein(NMP)havebeeninvestigatedinapromyelocyticleukemiccelllineHL-60inducedwithetoposide.BymeansofTUNELassay,thenucleidisplayedacharacteristicmorphologychange,andtheamountofapoptoticcellsincreasedearlyandreachedmaximunabout39%aftertreatmentwithetoposidefor2h.NucleosomalDNAfragmentationwasobservedaftertreatmentfor4h.ThemorphologicalchangeofHL-60cells,thus,occurredearlierthantheappearanceofDNAladder.Totalnuclearmatrixproteinswereanalyzedby2-dimensionalgelelectrophoresis.Differentialexpressionof59nuclearmatrixproteinswasfoundin4hetoposidetreatedcells.Westernblottingwasthenperformedonthreenuclearmatrixacssociatedproteins,PML,HSC70andNuMA.TheexpressionofthesuppressorPMLproteinandheatshockproteinHSC70weresignificantlyupregulatedafteretoposidetreatment,whileNuMA,anuclearmitoticapparatusprotein,wasdownregulated.Theseresultsdemonstratethatsignificantbiochemicalalterationsinnuclearmatrixproteinstakeplaceduringtheapoptoticprocess.