简介：组蛋白甲基化是参予细胞的过程的一个多样的数组的重要epigenetic现象并且被发现了与癌症被联系。几的Recentidentification嘘一demethylases证明了那嘘一甲基化是一个可逆过程。通过一条候选人途径，我们化学上有简历作为H3K27demethylase识别了JMJD3。进HeLa房间的JMJD3的Transfection引起了整齐的乙醇H3K27的特定的减小，但是没在di-和单音的甲基H3K27上有效果，或嘘H3K4和H3K9上的一离氨酸methylations。Theenzymatic活动要求JmjC域和被建议了为余因子绑定重要的保存组氨酸。试管内生物化学的实验证明那JMJD3directly催化demethylation。另外，我们发现JMJD3起来在前列腺癌症，和它的表示调整了在变形前列腺癌症是更高的。因此，我们作为能够把整齐的乙醇组从移开的ademethylase识别了JMJD3嘘一H3离氨酸27并且起来在前列腺癌症调整了。

简介：流行性感冒的所有已知的子类型A病毒在野水鸟被维持，这些病毒的自然水库。流行性感冒A病毒被孤立从许多有改变病态和死亡率的动物种类。更重要地，流行性感冒A病毒与潜在地致命的结果在人引起呼吸疾病。在人的本地或全球的爆发被过量住院和死亡典型地描绘。在1997，H5N1子类型的高度病原的鸟的流行性感冒病毒在传给人的香港出现了，导致由鸟的流行性感冒病毒感染的人的死亡的首先记录的盒子。在越南，印度尼西亚，和泰国在家禽在2003年7月开始的新爆发，和高度病原的鸟的H5N1流行性感冒病毒后来在整个亚洲并且进欧洲和非洲传播了。这些病毒继续与高死亡率感染人并且引起隐约可见的世界范围的担心流行。而且，H5N1病毒爆发在整个亚洲在家禽工业上有破坏效果。因为H5N1病毒爆发看起来从南部的中国发源，我们这里在中国检验H5N1流行性感冒病毒，与他们的生物性质上的一个重音。

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

简介：<正>Usingsubtractioncloning,weidentifiedthehumanN-MycDownstream-RegulatedGene-2(hNDRG2),locatedat14q11.2,asacandidatetumorsuppressorgene.Semi-quantitativeRT-PCRshowedthattheexpressionofhNDRG2in15of27(56%)humanGBMtissuesandall6humanglioblastomacelllineswassignificantlylowerthanthatinthenormalbrain.TheexpressionofhNDRG2alsowasevaluatedin60lung-carcinomapatients.17of26casesofsquamouscarcinomaand4of11casesofsmallcelllungcancerdisplayed

简介：GelatinaseA(MMP-2)isconsideredtoplayacriticalroleincellmigrationandinvasion.Theproteinaseiscercetedfromthecellasaninactivezymogen.InvivoitispostulatedthatactivationofprogelationaseA(proMMP-2)takesplaceonthecellsurfacemediatedbymembrane-typematrixmetalloproteinases(MT-MMPs).RecentstudieshavedemonstratedthatproMMP-2isrecruitedtothecellsurfacebyinteractingwithtissueinhibitorofmetalloproteinases-2(TIMP-2)boundtoMT1-MMPbyformingaternarycomplex.FreeMT1-MMPcloselylocatedtotheternarycomplexthenactivatesproMMP-2onthecellsurface.MT1-MMPisfoundinculturedinvasivecancercellsattheinvadopodia.TheMT-MMP/TIMP-2/MMP-2systemthusprovideslocalizedexpressionofproteolysisoftheextracellularmatrixrequiredforcellmigration.

简介：在哺乳动物的胚胎，内部房间团(ICM)的分离和trophectoderm(TE)的第一种房间命运选择，，被抄写因素，Oct4和Cdx2的互相对抗的效果调整pluripotency因素，Nanog，是必要的指定epiblast。我们分析了Nanog和Cdx2的倡导者，并且发现了这二个抄写因素同样相互地被调整。用有有条件的TE区别的一根胚胎的干细胞线，我们证明Nanogoverexpression压制TE标记的upregulation，当时Nanog击倒的upregulatesTE标记的表示。我们推进Nanog和Cdx2绑在并且镇压的表演对方的倡导者。而Nanog大美人在ICM导致可检测的Cdx2表示，我们不管多么不观察胚囊开发的公开混乱，显示Nanog起到在ICM和TE的分离的Oct4的一个谄媚的作用。

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简介：ErbB2,amemberofthereceptortyrosinekinasefamily,isfrequentlyover-expressedinbreastcancer.ProteolysisoftheextracellulardomainofErbB2resultsinconstitutiveactivationofErbB2kinase.RecentstudyreportedthatErbB2isfoundinthenucleus.Here,weshowedthatErbB2isimportedintothenucleusthroughanuclearlocalizationsignal(NLS)-mediatedmechanism.TheNLSsequenceKRRQQKIRKYTMRR(aa655-668)containsthreeclustersofbasicaminoacidsanditissufficienttotargetGFPintothenucleus.However,mutationinanybasicaminoacidclusterofthisNLSsequencesignificantlyaffectsitsnuclearlocalization.Furthermore,itwasfoundthatthisNLSisessentialforthenuclearlocalizationofErbB2sincetheintracellulardomainofErb2lackingNLScompletelyabrogatesitsnucleartranslocation.Takentogether,ourstudyidentifiedanovelnuclearlocalizationsignalandrevealsanovelmechanismunderlyingErbB2nucleartraffickingandlocalization.

简介：包括谷物尺寸和圆锥花序形态学，圆锥花序的建筑学直接决定谷物产量。圆锥花序直立，为在中国的北部分完成理想的植物建筑学被选择，引起了米饭breeders的增加的注意。这里，稠密、直立的圆锥花序2(dep2)异种，显示出稠密、直立的圆锥花序显型，被识别。没有任何已知的功能的领域，DEP2编码植物特定的蛋白质。表示介绍DEP2表明它高度在年轻纸巾被表示，与在年轻圆锥花序的大多数丰富。词法并且表示分析显示在DEP2的那个变化主要影响脊柱和主要、第二等的分支的快速的延伸，但是不损害圆锥花序primordia的开始或形成。进一步的分析建议在dep2的圆锥花序长度的减少被一个缺点在圆锥花序的指数的延伸期间在房间增长引起。尽管有在dep2异种的一种更紧缩的植物类型，在谷物生产的重要改变都没在野类型和dep2异种之间被发现。因此，DEP2的学习不仅加强我们圆锥花序建筑学的分子的基因基础的理解而且为米饭繁殖有重要含意。

简介：One-cellmouseembryosfromKMstrainandB6C3F1strainwereculturedinM16medium,inwhich2-cellblockgenerallyoccurs.EmbryosofKMstrainexhibited2-cellblock,whereasB6C3F1embryos,whichareregardedasanonblockingstrain,proceededtothe4-cellstageinourculturecondition.Itisoftenassumedthattheblockofearlydevelopmentisduetothefailureofzygoticgeneactivation(ZGA)inculturedembryos.Inthisstudyweexaminedproteinsynthesispatternsbytwo-dimensionalgelelectrophoresisof[35S]methionineradiolabeled2-cellembryos.Embryosfromtheblockingstrainandthenonblockingstrainwerecomparedintheirdevelopmentbothinvitroandinvivo.ThedetectionofTRCexpression,amarkerofZGA,at42hposthCGinKMembryosdevelopedinvitrosuggestedthatZGAwasalsoinitiatedeveninthe2-cellarrestedembryos.Nevertheless,asignificantdelayofZGAwasobservedinKMstrainascomparedwithnormallydevelopedB6C3F1embryos.AttheverybeginningofmajorZGAasearlyas36hposthCG,TRChasalreadybeenexpressedinB6C3F1embryosdevelopedinvitroandKMembryosdevelopedinvivo.Butfor2-cellblockedKMembryos,TRCwasstillnotdetectableevenat38hposthCG.Theseevidencessuggestthat2-cell-blockedembryosdoinitiateZGA,andthat2-cellblockphenomenonisduenottothedisabilityininitiatingZGA,buttoadelayofZGA.

简介：Inordertostudythemechanismoftheeffectofheparinonapoptosisincarcinomacells,thenasopharyngealcarcinomacelllineCNE2wasusedtoidentifytheeffectofheparinonapoptosisassociatedwiththeexpressionofc-myc,bax,bcl-2proteinsbyuseofHoechst33258staining,terminaldeoxynucleotidyltransferase-mediateddUTPnick-endlabeling(TUNEL),agarosegelelectrophoresis,andflowcytometry,aswellasWesternblotanalysis.TheresultsshowedthatheparininducedapoptosisofCNE2cellsincludingthemorphologicchangessuchasreductioninthevolume,andthenuclearchromatincondensation,aswellasthe“ladderpattern”revealedbyagarosegelelectrophoresisofDNAinaconcentration-dependentmanner.ThenumberofTUNEL-positivecellswasdramaticallyincreasedto33.6±1.2%from2.8±0.3%bytreatmentwithheparinindifferentconcentrations(10～40kU/L).Theapoptoticindexwasincreasedto32.5%from3.5%bydetectingSubG1peaksonflowcytometry.Westernblotanalysisshowedthatlevelsofbcl-2,baxandc-mycweresignificantlyoverexpressedbytreatmentwiththeincreaseofheparinconcentrations.TheseresultssuggestthatheparininducesapoptosisofCNE2cells,whichmayberegulatedbydifferentialexpressionofapoptosis-relatedgenes.

简介：导致死亡的肿瘤坏死的能力因素相关的导致apoptosisligand(小道)大部分被描述了有选择地杀死许多癌症房间，但是有治疗的主要担心之一是药抵抗和可能的有毒的副作用的出现。这里，我们报导那条小道在Jurkat和SUPT1T房间线并且在人的高强风然而并非在健康的导出题目的外部血mononuclear房间导致apoptosis。在平行，有小道和Tyrphostin(AG-490)的治疗，选择Januskinase2禁止者，生产cytotoxicity的明显的改进，与控制相比或到由Stat3phosphorylation的重要抑制描绘了落后于独自一个对待的样品，并且与cIAP-1和cIAP-2mRNA层次的戏剧的减少联系了。由特定的小干扰RNA的cIAP-1和cIAP-2的Downregulation显著地放大减少小道的cytotoxicity。所有一起，这些调查结果强烈显示cIAP-1和cIAP-2downregulation是在调停的发信号的小径的基本的步T上的小道和AG-490的组合效果房间白血病。这些调查结果可以帮助在小道敏感的白血病影响的病人的治疗为不太有毒的药理学策略的发展打开新线路。

简介：Apoptosismanifestsintwomajorexecutionprogramsdownstreamofthedeathsignal:thecaspasepathwayandorganelledysfunction.Animportantantiapoptosisfactor,Bcl-2protein,contributesincaspasepathwayofapoptosis.Calcium,animportantintracellularsignalelementincells,isalsoobservedtohavechangesduringapoptosis,whichmaybeaffectedbyBcl-2protein.WehavepreviouslyreportedthatinHarringtonine(HT)inducedapoptosisofHL-60cells,there'schangeofintracellularcalciumdistribution,ovingfromcytoplastespeciallyGolgi'sapparatustonucleusandaccumulatingtherewiththehighestconcentration.Wereportherethatcaspase-3becomesactivatedinHT-inducedapoptosisofHL-60cells,whichcanbeinhibitedbyoverexpressionofBcl-2protein.NosignofapoptosisorintracellularcalciummovementfromGolgi'sapparatustonucleusinHL-60cellsoverexpressingBcl-2ortreatedwithAc-DEVD-CHO,aspecificinhibitorofcaspase-3.Theresultsindicatethatactivatedcaspase-2canpromotethemovementofintracellularcalciumfromGolgi'sapparatustonucleus,andtheprocessisinhibitedbyAc-DEVD-CHO(inhibitorofcaspase-3),andthatBcl-2caninhibitthemovementandaccumulationofintracellularcalciuminnucleusthroughitsinhibitiononcaspase-3.Calciumrelocalizationinapoptosisseemstobeirreversible,whichisdifferentfromtheintracellularcalciumchangescausedbygrowthfactor.

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简介：Polyamines在在植物，而是他们的准确角色调整各种各样的发展过程被含有并且他们怎么管理这些过程尚待逃犯。我们这里报导浓密的Arabidopsis和矮子异种，bud2，哪个从编码S-adenosylmethioninedecarboxylases(SAMDC)的小基因家庭的一个成员的完全的删除的结果为在polyamine简历的不可缺少的中介的形成必要合成小径。bud2植物在开花期，根，和叶柄扩大了脉管的系统，并且polyamines的改变的动态平衡。bud2和samdc1的双异种，另一个SAMDC成员的击倒的异种，是胚胎致命，证明SAMDC为植物胚胎开始是必要的。我们的结果建议polyamines为更高的植物的正常生长和发展被要求。

简介：MicroRNAs是否定地在post-transcriptional水平调制基因表示的短规章的RNA，并且深深地涉及癌症的几种类型的致病。调查特定的miRNAs和他们的目标基因是否参予喉的癌的分子的致病，oligonucleotidemicroarrays被用来与正常纸巾相比在喉的癌纸巾估计microRNAs和mRNAs的微分表示侧面。oncogenicmiRNA，microRNA-21(miR-21)，被发现是在喉的癌纸巾的upregulated。由特定的antisenseoligonucleotides的miR-21击倒而miR-21的overexpression提高了细胞的生长活动，由殖民地形成试金检测了，禁止了HEp-2细胞的增长潜力。miR-21抑制引起的房间数字减小由于G1-S阶段转变的控制的损失，而不是apoptosis的显著增加。随后，miR-21的新目标基因，BTG2，被发现是在喉的癌纸巾的downregulated。BTG2被知道充当一个平底锅房间周期管理者和肿瘤suppressor。这些调查结果显示miR-21的那异常表情可以由维持BTG2的底层贡献喉的癌的恶意的显型。oncogenicmiR-21和它的目标基因的鉴定，BTG2，为癌症诊断和治疗在喉的癌是潜在地珍贵的。

简介：Apoptosisplaysanimportantroleinembryonicdevelopment,tissueremodeling,immuneregulationandtumorregression.Twogroupsofmolecules(Bcl-2familyand“Deathfactor”family)areinvolvedinregulatingapoptosis.InordertoknowabouttheeffectofBcl-2onapoptosisinducedbyFas,atypicalmemberof“Deathfactor”family,thetransfectionexperimentswithexpressionvectorspcDNA3-flandpcDNA3-bcl-2wereperformedinBEL-7404cells,ahumanhepatocellularcarcinomacelllinewhichexpressesendogenousFas,butnotFasLandBcl-2.ThedatashowedthattheexpressionofFasLinpcDNA3-fltransfectedhepatomacellsobviouslyinducedtheapoptosisofthecells.However,theoverexpressionofBcl-2inpcDNA3-bcl-2transfected7404/b-16cellscounteractedpcDNA3-fltransienttransfectionmediatedapoptosis.FurtherstudybycotransfectionexperimentsindicatedthatBidbutnotBax(bothwerepro-apoptoticproteinsofBcl-2family)blockedtheinhibitoryeffectofBcl-2onFas-mediatedapoptosis.TheseresultssuggestedthatFas-mediatedapoptosisinhumanhepatomacellsispossiblyregulatedbyBcl-2familyproteinsviamitochondriapathway.

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