简介：叶绿体是从endosymbioticcyanobacteria演变的植物特定的细胞器。他们通过二进制分裂划分。叶绿体部门地点的选择为对称的叶绿体部门是枢轴的。在E。coli，在房间的中点部门地点放被Min系统的动态摆动调整，它包括MinC，头脑和矿。在植物的头脑和矿的相当或相同的事物涉及叶绿体分割。MinC的相当或相同的事物仍然没在更高的植物被识别。然而，象FtsZ一样蛋白质，ARC3，被发现地点放涉及叶绿体分割。这里，我们报导放1的那个叶绿体部门地点(AtCDP1)是在Arabidopsis涉及叶绿体部门地点放置的新奇叶绿体部门蛋白质。AtCDP1被与房间部门显型为殖民地在细菌屏蔽一个ArabidopsiscDNA表示图书馆发现。AtCDP1只在Arabidopsis在年轻绿纸巾被表示。有多重部门地点的伸长的叶绿体在loss-of-functioncdp1异种被观察。AtCDP1的Overexpression也引起了一个叶绿体部门显型。蛋白质相互作用试金建议AtCDP1可以调停通过和ARC3的相互作用放的叶绿体部门地点。总的来说，我们的结果显示AtCDP1是放系统，和这个系统的工作机制的叶绿体部门地点的一个新奇部件与在原核生物的房间的传统的MinCDE系统的不同。

简介：P28，a28kDproteinfromtoad(Bufobufogargarizans)oocytes,wasidentifiedbyusingP13^suc1-agaroseaffinitychromatography.Sequencehomologyanalysisofthefull-lengthcDNAofP28(GeneBankaccessionnumber:AF314091)indicatedthatitencodesaproteincontaining224amino-acidswithabout55%iden-titiesandmorethan70%positivestoencodesaproteincontaining224amino-acidswithabout55%iden-titiesandmorethan70%positivestohuman,ratormouseUCH-L1,andcontainshomologicalfunctionaldomainsofUCHfamily.Anti-p28monoclonalantibody,oninjectingintotheoocytes,couldinhibittheprogesterone-inducedresumptionofmeioticdivisioninadose-dependentmanner.TherecombinantproteinP28showedsimilarSDS/PAGEbehaviorstothenativeone,andpromotedubiquitinethylesterhydrolysis,aclassicalcatalyticreactionforubiquitincarboxylterminalhydrolases(UCHs).Theresultsinthispaperrevealthatanovelprotein,p28,existsinthetoadoocytes,isaUCHLlhomolog,wasengagedintheprocessofprogesterone-inducedoocytematurationpossiblythroughaninvolvementinproteinturnoveranddegradation.

简介：γ-AminobutyricacidandGABAergicreceptorswerepreviouslyreportedtobedistributedinreproductivesystemsbesidesCNSandpredictedtoparticipateinthemodulationoftesticularfunction.γ-Aminobutyricacidtransporterwasimplicatedtobeinvolvedinthisprocess.However,thepotentialroleofγ-aminobutyrictransporterintestishasnotbeenexplored.Inthisstudy,weinvestigatedtheexistenceofmouseγ-aminobutyricacidtransportersubtypeI(mGAT1)intestis.Wild-typeandtransgenicmice,whichoverexpressingmGAT1inavarietyoftissues,especiallyintestis,wereprimarilystudiedtoapproachtheprofileofmGAT1intestis.MicewithoverexpressedmGAT1developnormallybutwithreducedmassandsizeoftestisascomparedwithwild-type.Testicularmorphologyoftransgenicmiceexhibitedovertabnormalitiesincludingfocaldamageofthespermatogenicepitheliumaccompaniedbycapillariesproliferationandincreaseddiameterofseminiferoustubuleslumen.Reducednumberofspermatidswasalsofoundinsomeseminiferoustubules.OurresultsclearlydemonstratethepresenceofGAT1inmousetestisandimplythatGAT1ispossiblyinvolvedintesticularfunction.

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：ASK1(ARABIDOPSIS象SKP1一样)蛋白质是招募的ubiquitinligase建筑群指向的SCF(Skp1-Cullin-F盒子蛋白质)的一个批评部件为由26Sproteosome的降级的蛋白质。为了调查蛋白质，那被调停ASK1的解朊作用小径在Arabidopsis花影响，我们用二维的电气泳动(2-DE)比较了Arabidopsis野类型和ask1异种花芽的proteomes。有在与野类型花相比的ask1异种花的更高或更低的丰富的十个蛋白质点被切除并且使分析遭到了到进一步集体的spectrometry(MS)。结果证明他们是涉及相片形态发生，生理节奏的摆动，翻译以后的过程，压力反应和房间扩大或延伸的蛋白质，建议那些过程在ask1异种被影响。基因也是的这些的抄本层次基于Affymetrix基因芯片比较了微数组数据。没有重要差别为大多数基因被观察，建议有在ask1异种的累积的提高的层次的蛋白质能是一条调停ASK1的解朊作用小径调整的候选人目标。阐明的这些结果帮助在Arabidopsis发展过程并且也的ASK1的多种的功能表明关于基因功能学习蛋白质层次的重要性和必要性。

简介：Activehost-pathogeninteractionstakeplaceduringinfectionofhumanimmunodeficiencyvirustype1(HIV-1).Outcomesoftheseinteractionsdeterminetheefficiencyofviralinfectionandsubsequentdiseaseprogression.HIV-infectedcellsrespondtoviralinvasionwithvariousdefensivestrategiessuchasinnate,cellularandhumoralimmuneantiviralmechanisms.Ontheotherhand,thevirushasalsodevelopedvariousoffensivetacticstosuppressthesehostcellularresponses.Amongmanyoftheviraloffensivestrategies,HIV-1viralauxiliaryproteins(Tat,Rev,Nef,Vif,VprandVpu)playimportantrolesinthehost-pathogeninteractionandthushavesignificantimpactsontheoutcomeofHIVinfection.OneofthebestexamplesistheinteractionofVifwithahostcytidinedeaminaseAPOBEC3G.AlthoughspecificrolesofotherauxiliaryproteinsarenotaswelldescribedasVif-APOBEC3Ginteraction,itisthegoalofthisbriefreviewtosummarizesomeofthepreliminaryfindingswiththehopetostimulatefurtherdiscussionandinvestigationinthisexhilaratingareaofresearch.

简介：真核细胞的房间的最惹人注目的形态特征是各种各样的围住膜的分隔空间的存在。包括细胞器和短暂运输中介，这些分隔空间不是静态的。更确切地说，蛋白质和膜的动态交换被需要维持细胞的动态平衡。膜动员的最戏剧的例子之一在macroautophagy的过程期间被看见。Macroautophagy是为长寿蛋白质和细胞器的降级的主要细胞的小径。响应环境暗示，例如饥饿或应力的另外的类型，房间生产唯一的膜结构，phagophore.Thephagophore扣押它形成一个双膜cytosolic泡的细胞质，anautophagosome。在结束之后，autophagosome与溶酶体熔化或在酵母的一个液泡，它交付水疗院放射激光与它的货物，和产生大分子一起毁坏内部autophagosome膜回来被释放进cytosol因为reuse.Autophagy因此是正在骑车过程，允许房间熬过滋养的限制的时期；然而，它有一个更宽的生理的角色，参予开发和老化，并且另外在对病原体侵略，癌症和某些neurodegenerative的保护疾病。在许多情况中，autophagy的角色通过autophagy相关的蛋白质的研究被识别，Atg6/Beclin1。这蛋白质是类脂化合物kinase建筑群的部分，并且最近的研究建议它在协调autophagy并且在反对apoptosis的细胞的死亡过程的thecytoprotective功能起一个中央作用。这里，我们总结我们Atg6/Beclin的当前的知识1在在细胞的不同模型有机体和它的唯一的功能。

简介：ToexplorethemolecularmechanismofchromatinremodelinginvolvedintheregulationoftranscriptionalactivationofspecificgenesbyamyogenicregulatoryfactorMyogenin,weusedNIH3T3fibroblastswithastablyintegratedH1.1-GFPfusionproteintomonitorhistoneH1movementdirectlybyfluorescencerecov-eryafterphotobleaching(FRAP)inlivingcells.TheobservationfromFRAPexperimentswithmyogenintransfectedfibroblastsshowedthattheexchangerateofhistoneH1inchromatinwasobviouslyincreased,indicatingthatforcedexpressionofexogenousMyogenincaninducechromatinremodeling.Thehyper-acetylationofhistonesH3andH4frommyogenintransfectedfibroblastswasdetectedbytriton-acid-urea(TAU)/SDS(2-D)electrophoresisandWesternblotwithspecificantibodiesagainstacetylatedN-terminiofhistonesH3andH4.RT-PCRanalysisindicatedthatthenAChRa-subunitgenewasexpressedinthetrans-fectedfibroblasts.TheseresultssuggestthattheexpressionofexogenousMyogenincaninducechromatinremodelingandactivatethetranscriotionofMvogenin-targetedgeneinnon-musclecells.

简介：干扰素规章的因素(IRF)3在病毒或细菌的侵略期间为chemokines和cytokines的transcriptional正式就职是批评的。kinases坦克有约束力的kinase(TBK)1并且IkappaBkinase(IKK)蔚罐头phosphorylateIRF3和玩的C终端部分在IRF3激活的重要角色。在这研究，我们显示出那另外一个kinase，c-Jun-NH2-terminalkinase(JNK)，它的N终端丝氨酸上的phosphorylatesIRF3173残余，和TAK1能经由JNK刺激IRF3phosphorylation。没有影响C终端phosphorylation，JNK特定的禁止者SP600125禁止N终端phosphorylation。另外，lipopolysaccharide(LPS)上的调停IRF3的基因表情或polyinosinic-cytidylic酸(polyI:C)处理被SP600125严重地损害，以及为IRF3激活的记者基因试金。进一步证实的TAK1击倒这些观察。有趣地，组成的活跃IRF3(5D)能被SP600125禁止；JNK1罐头synergizeIRF3(5D)的行动，然而并非S173A-IRF3(5D)变异。更重要地，polyI:没能戏剧性地导致变异的S173A和SP600125的phosphorylation的C废除了被polyI刺激的IRF3phosphorylation和dimerization:C。因此，这研究证明TAK1-JNK串联为IRF3功能被要求，除了TBK1/IKK蔚，揭开为激活mitogen的蛋白质(地图)的新机制调整天生的免疫的kinase。

简介：Inmacrophages,theaccumulationofcholesterylesterssynthesizedbytheactivatedacyl-coenzymeA:cholesterolacyltransferase-1(ACAT1)resultsinthefoamcellformation,ahallmarkofearlyatheroscleroticlesions.Inthisstudy,withthetreatmentofaglucocorticoidhormonedexamethasone(Dex),lipidstainingresultsclearlyshowedthelargeaccumulationoflipiddropletscontainingcholesterylestersinTHP-1-derivedmacrophagesexposedtolowerconcentrationoftheoxidizedlow-densitylipoprotein(ox-LDL).Morenotably,whentreatedtogetherwithspecificanti-ACATinhibitors,theabundantcholesterylesteraccumulationwasmarkedlydiminishedinTHP-l-derivedmacrophages,confirmingthatACATisthekeyenzymeresponsibleforintracellularcholesterylestersynthesis.RT-PCRandWesternblotresultsindicatedthatDexcausedup-regulationofhumanACAT1expressionatboththemRNAandproteinlevelsinTHP-1andTHP-1-derivedmacrophages.TheluciferaseactivityassaydemonstratedthatDexcouldenhancetheactivityofhumanACAT1geneP1promoter,amajorfactorleadingtotheACAT1activation,inacell-specificmanner.Furtherexperimentalevidencesshowedthataglucocorticoidresponseelement(GRE)locatedwithinhumanACAT1geneP1promotertoresponsetotheelevationofhumanACAT1geneexpressionbyDexcouldbefunctionallyboundwithglucocorticoidreceptor(GR)proteins.ThesedatasupportedthehypothesisthattheclinicaltreatmentwithDex,whichincreasedtheincidenceofatherosclerosis,mayinpartduetoenhancingtheACAT1expressiontopromotetheaccumulationofcholesterylestersduringthemacrophage-derivedfoamcellformation,anearlystageofatherosclerosis.

简介：门高血压(PHT)gastropathy是肝肝硬化的经常的复杂并发症，带之一从肝硬化死亡引起。Apoptosis广泛地被认为从坏死的房间死亡是房间死亡和一个不同实体的一个活跃精力依赖者模式。胃的mucosalapoptosis是否涉及PHTgastropathy，是不清楚的。通过cyclooxygenase(艇长)生产的前列腺素(PG)被认为从损害和apoptosis在胃肠的mucosa的保护起一个关键作用。然而，在PHTgastropathy的艇长的角色仍然不清楚地被理解。这研究的目的是调查(1)胃的mucosalapoptosis是否涉及PHTgastropathy，(2)艇长的downregulation贡献这apoptosis。在这研究，当mucosal增长在PHT老鼠被禁止时，我们证明胃的mucosalapoptosis显著地被增加。胃的mucosalCOX-1显著地在mRNA和蛋白质层次被压制，并且PGE2在PHT老鼠被减少。进一步，PGE2处理在PHT老鼠压制了胃的mucosalapoptosis。然而，胃的mucosalCOX-2层次没在假冒操作老鼠和PHT老鼠之间不同。肿瘤坏死因素的胃的mucosal层次--(TNF-)并且船边交货ligand，然而并非TNF相关的导致apoptosisligand，被增加，并且激活的caspase-8和caspase-3层次是在PHT老鼠的upregulated。到cytosol的从线粒体的细胞色素c的版本没在PHT老鼠被观察。我们的数据显示COX-1的downregulation经由死亡涉及胃的mucosalapoptosis调停信号的类型--我在PHT老鼠的房间死亡。

简介：WereportedinthismanuscriptthatTGF-β1inducesapoptosisinAML12murinehepatocytes,whichisassociatedwiththeactivationofp38MAPKsignalingpathway.SB202190,aspecificinhibitorofp38MAPK,stronglyinhibitedtheTGF-β1-inducedapoptosisandPAI-1promoteractivity.TreatmentofcellswithTGF-β1activatesp38.Furthermore,over-expressionofdominantnegativemutantp38alsoreducedtheTGF-β1-inducedapoptosis.Thedataindicatethattheactivationofp38isinvolvedinTGF-β1-mediatedgeneexpressionandapoptosis.

简介：兼容丑恶纸巾的表面上的花粉萌芽是为植物授精的必要的步。这里，我们报导Arabidopsis变异的bcl1是由于花粉萌芽的失败不育的男性。我们证明bcl1异种等位基因不能被男配偶体播送，没有同型结合的bcl1异种被获得。花粉发育阶段的分析显示bcl1变化影响花粉萌芽然而并非花粉成熟。分子的分析证明花粉萌芽的失败被AtBECLIN1的混乱引起。AtBECLIN1在成熟花粉主要被表示并且与重要相同编码蛋白质到在酵母为autophagyandvacuolar蛋白质排序的过程(VPS)要求的Beclin1/Atg6/Vps30。我们也证明AtBECLIN1为正常被要求植物开发，和那与autophagy，VPS和glycosylphosphatidylinositolanchor系统有关的基因，被AtBECLIN1的缺乏影响。

简介：MembersofBcl-2familyofproteinsareregulatorsofcelldeaththatcanbegroupedintosubfamiliesofprosurvivalandproapoptoticmolecules.Theyarecharacterizedbythepresenceofseveralconservedmotifs,knownastheBcl-2homology(BH)domains,designatedBH1,BH2,BH3andBH4.MutagenesisandstructuralstudiesrevealedthattheBHdomainsareimportantfunctionaldomainsthatarealsorequiredfordimerizationfunction.Recently,asubfamilyofproapoptoticmoleculesonlycontainsBH3motifhasbeenidentifiedsuggestingBH3domainalonemaybesufficientformediatingproapoptoticfunctionamong

简介：Peroxisome激活proliferator的受体鲸鱼群妈(PPARγ)coactivator-1高山哈(PGC-1α)coactivates多重抄写因素并且调整几个代谢过程。Thecurrent学习在人的上皮的卵巢的癌症房间在apoptosis的正式就职调查了PGC-1α的角色。在人的卵巢和人的卵巢的上皮的肿瘤之间的PGC-1α信使rna水平被量的RT-PCR检验。更少的PGC-1α表示与正常卵巢相比在恶意的肿瘤的表面上皮被发现。在人的上皮的卵巢的癌症房间线Ho-8910的PGC-1α的Overexpression通过Bcl-2和Bax表示的协调规定导致了房间apoptosis。Microarray分析证实PGC-1α戏剧性地在Ho-8910房间影响了apoptosis相关的基因。Mitochondrial功能的试金证明apoptosis的正式就职通过由细胞色素c.Furthermore的版本的终端阶段，导致的apoptosis部分是，然而并非完全，由PPARγantagonist(GW9662)堵住了的PGC-1α-，并且由siRNA的PPARγ表示的抑制也在Ho-8910房间禁止了PGC-1α-inducedapoptosis。这些数据建议PGC-1α通过aPPARγ-依赖者小径施加了它的效果。我们的调查结果显示PGC-1α涉及apoptoticsignaltransduction小径，PGC-1α的down规定可以是在支持上皮的卵巢的癌症生长和前进的一个关键点。

简介：

简介：TRAF2isacriticaladaptormoleculeforTNFreceptorsininflammatoryandimmunesignaling.Uponreceptorengagement,TRAF2isrecruitedtoCD40andtranslocatestolipidraftsinaRINGfinger-dependentprocess,whichenablestheactivationofdownstreamkinases.TRAF1candisplaceTRAF2andCD40fromraftfractions,anditpromotestheabilityofTRAF2tosustainsignalactivation.ReplacementoftheRINGfingerofTRAF2witharaft-targetingsignalrestoresJNKactivationandassociationwiththecytoskeletalproteinFilamin,butnotNF-KBactivation.TRAF1-/-dendriticcellsshowattenuatedresponses

简介：Ionizingradiationisoneofthemosteffectivetoolsincancertherapy.Inapreviousstudy,wereportedthatproteintyrosinekinase(PTK)inhibitorsmodulatetheradiationresponsesinthehumanchronicmyelogenousleukemia(CML)celllineK562.Thereceptortyrosinekinaseinhibitor,genistein,delayedradiation-inducedcelldeath,whilenon-receptertyrosinekinaseinhibitor,herbimycinA(HMA)enhancesradiation-inducedapoptosis.Inthisstudy,wefocusedonthemodulationofradiation-inducedcelldeathbygenisteinandperformedPCR-selectsuppressionsubtractivehybridization(SSH)tounderstanditsmolecularmechanism.Weidentifiedhumanthymidinekinase1(TK1),whichiscellcycleregulatorygeneandconfirmedexpressionofTK1mRNAbyNorthernblotanalysis.ExpressionofTK1mRNAandTK1enzymaticactivitywereparallelintheirincreaseanddecrease.TK1isinvolvedinG1-Sphasetransitionofcellcycleprogression.Incellcycleanalysis,weshowedthatradiationinducedG2arrestinK562cellsbutitwasnotabletosustain.However,theadditionofgenisteintoirradiatedcellssustainedaprolongedG2arrestupto120h.Inaddition,theexpressionofcellcycle-relatedproteins,cyclinAandcyclinB1,providedtheevidencesofG1/SprogressionandG2-arrest,andtheirrelationshipwithTK1incellstreatedwithradiationandgenistein.TheseresultssuggestthattheactivationofTK1maybecriticaltomodulatetheradiation-inducedcelldeathandcellcycleprogressioninirradiatedK562cells.

简介：Wntsignalingplaysanimportantroleinembryogenesisandtumorgenesis.AlthoughthemechanismabouthowWntstransducetheirsignalingfromreceptorfrizzled(Fz)tocytosolhasnotbeenunderstood,dishevelled(Dvl)proteinwasconsideredastheintersectionofWntsignaltraffic.Inthisstudy,wecharacterizedthefunctionofthreedomains(DIX,PDZandDEP)ofDvl-1incanonicalWntsignaltransductionandDvl-1membranetranslocation.ItwasfoundbothDIXandDEPdomainweresufficienttoblockWnt-3a-inducedLEF-1transcriptionalactivityandfreecytosolβ-cateninaccumulation;whereasPDZdomainandafunctionalmutantformofDEPdomain(DEP-KM)hadnoeffectoncanonicalWntsignaling.Inaddition,whencotransfectedwithFz-7,DEPdomain,butnotDIX,PDZorDEP-KM,translocatedandco-localizedwithFz-7totheplasmamembrane,whichwassimilartoDvl-1.Furthermore,itwasDEPdomainthatcouldblockFz-7-inducedmembranetranslocationofDvl-1viaapossiblecompetitivemechanism.TheseresultsstronglysuggestthatDEPdomainisresponsibleforthemembranetranslocationofDvl-1proteinuponWntsignalstimulation.

简介：Amajorproblemwhichispoorlyunderstoodinthemanagementofbladdercancerislowsensitivitytochemotherapyandhighrecurrenceaftertransurethralresection.Insulin-likegrowthfactor1receptor(IGF-1R)signalingplaysaveryimportantroleinprogression,invasionandmetastasisofbladdercancercells.Inthisstudy,weinvestigatedwhetherIGF-1Rwasinvolvedinthegrowthstimulatingactivityanddrugresistanceofbladdercancercells.Theresultsshowed:ThemRNAsofIGF-1,IGF-2andIGF-1Rwerestronglyexpressedinserum-freeculturedT24cellline,whereasnormalurothelialcellsdidnotexpressthesefactors/receptorsoronlyintracelevels;T24cellrespondedfarbettertogrowthstimulationbyIGF-1thandidnormalurothelialcells;blockageofIGF1Rbyantisenseoligodeoxynucleotide(ODN)significantlyinhibitedthegrowthofT24cellandenhancedsensitivityandapoptosisofT24cellstomitomycin(MMC).TheseresultssuggestedthatblockageofIGF-IRsignalingmightpotentiallycontributetothetreatmentofbladdercancercellswhichareinsensitivetochemotherapy.