简介：Mammaliancelltotipotencyisasubjectthathasfascinatedscientistsforgenerations.AlonglastingquestionwhethersomeofthesomaticcellsretainstotipotencywasansweredbythecloningofDollyattheendofthe20thcentury.Thedawnofthe218thasbroughtforwardgreatexpectationsinharnessingthepoweroftotipotentcyinmedicine.Throughstemcellbiology,itispossibletogenerateanypartsofthehumanbodybystemcellengineering.Considerableresourceswillbedevotedtoharnesstheuntappedpotentialsofstemcellsintheforeseeablefuturewhichmaytransformmedicineasweknowtoday.Atthemolecularlevel,totipotencyhasbeenlinkedtoasingulartranscriptionfactoranditsexpressionappearstodefinewhetheracellshouldbetotipotent.NamedOct4,itcanactivateorrepresstheexpressionofvariousgenes.Curiously,verylittleisknownaboutOct4beyonditsabilitytoregulategeneexpression.ThemechanismbywhichOct4specifiestotipotencyremainsentirelyunresolved.Inthisreview,wesummarizerethestructureandfunctionofOct4andaddresstoOct4functioninmaintainingtotipotencyorpluripotencyofembryonicstemcels.

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简介：Thebindingofnuclearproteinspreparedfrommouseerythroidtissueindifferentdevelopmentalstagestothe5'-flankingregulatoryelementsofhumanβ-globingene,twonegativecontrolregions(NCR1,-610to-490bp;NCR2,-338,to-233bp),wasidentified.TwostagespecificproteinfactorscorrespondingtoembryonicandfetalstageswerefoundtobecapableofbindingtoNCR2.Thesedataprovidedevidencethatthecisactingelementsofthe5'-flankingregionmightbeinvolvedinthedevelopmentalcontrolofβ-globingeneandNCR2mightberesponsibleinartforthesilenceofβ-glolbingeneintheembryonicandfetalstages.

简介：MicroRNAs(miRNA)指导在基因表示的一个重要角色在植物为到环境条件的发展进程和回答要求了的顺序特定的posttranscriptional基因silencing玩。然而，很少对transcriptional和miRNA表示的posttranscriptional规定被知道。Histoneacetylation在染色质改变起一个重要作用并且为基因激活被要求。由在Arabidopsis的异种分析miRNAs和相应主要miRNAs的子集的累积，我们显示出那histoneacetyltransferaseGCN5(一般控制非镇压的protein5)在miRNA上有一般压抑的效果生产，当它为一个子集的表示被要求时(例如压力可诱导)MIRNA基因。在miRNA生产的GCN5的一般否定功能多半通过象DICERLIKE1(DCL1)那样的miRNA机械基因的间接压抑被完成，有锯齿(SE)，偏下性的LEAVES1(HYL1)和ARGONAUTE1(AGO1)。染色质immunoprecipitation试金表明GCN5指向到MIRNA基因的一个子集并且为在这些loci的histoneH3离氨酸14的acetylation被要求。而且，由trichostatin的histonedeacetylation的抑制一个处理或在histonedeacetylase，基因异种损害了某些miRNAs的累积。这些数据一起建议ArabidopsisGCN5在transcriptional和posttranscriptional层次防碍miRNA小径，histoneacetylation/deacetylation是涉及miRNA的规定的epigenetic机制生产。

简介：Xenopusorganizerspecificgenenogginpossessesnearlyallthecharacteresticpropertiesoftheactionoforganizertospecifytheembryonicbodyacis.Toanalyzehowthematernalinheritedfactorscontrolitsexpressionpattern,weclonedthe5'regulatoryregionofnoggingene.The1.5kbupstreamsequensecoulddirectreportergenetoexpressinvivoanddatafromdeletionanalysisindicatedthata229basepairfragmetisessentialforactivatingnogginexpression.WefurtherdemonstratedthattheresponseelementswithinthisregulatoryregionwereindeedunderthecontrolofgrowthfactoractivinandWntsignalingpathwaycomponents.

简介：InteractionbetweencytotoxicTlymphocyte-associatedantigen-4(CTLA4,CD152)andB7molecules(B7-1andB7-2)isofimportanceinthecellulareventsoflymphocyte,includingantigen-specificT-cellactivationandinductionofautoreactiveT-cell.WedescribehaerethefirstintroductionofamurinesolubleCTLA4gene,CTLA4Ig,toMm1cells,amacrophagiccellline.CTLA4IgwassuccessfullyexpressedonMm1cellsandtheexpressedCTLA4IgwasfoundtobefunctionallyactiveintheirbindingtoB7moleculesbyflowcytometryandimmunofluorescencestudies.ThebiologicalactivityofCTLA4IgfromthetransfectedMm1cellswasstudiedandshowedinhibitoryactivityonmixedlymphocyteculture.AhighCTLA4Igproducingmacrophagiccelllinewasobtained.AsMm1cellswereregardedasdifficultforgenetransfectionandtherehassofarbeennoreportonexpressionofCTLA4IggeneonMm1cells,theseresultssuggestedthattheCELA4IgexpressingMm1cellscouldbeusefulforanalysisofCTLA4andB8moleculeinteractioninbothmacrophageandT-cell.

简介：Trichosanthin(TCS)isapotentallergentomice.Accordingtoourpreviousexperiments,itcouldbringouttheIgEresponsetoovabumin(OVA)ifTCSwasgivenonedaybeforeOVAimmunization,whileOVAalonecouldnotinduceIgEtoit.Inthiswork,thekineticsofinterleukin4(IL-4)andinterferonγ(IFN-γ)geneexpressioninthemesentericlymphnode(MLN)ofTCS-immunizedmicewasinvestigatedusingasemi-quantitativeRT-PCRmethod.ItindicatedthatTCSinducedsignificantIL-4geneexpressionandthepeaksofIL4geneexpressionwereondayoneafterTCSimmunizationinbothprimaryandsecondaryresponse.Incontrast,theIFN-γgeneexpressionwassuppressed.Furthermor,theIL-4geneexpressioninthesecondaryresponsewaslowerthanthatintheprimaryresponse.ThusthepresenceofIgEmemoryBcellswerestudied.ResultsshowedthattheamountofmatureIgEmRNAarosesignificantlyandrapidlyonedayafterTCSrestimulation,whileintheMLNofthemiceprimed30daysbeforeandwithoutboost,itwasalmostasthesameamountoftheunimmunizedcontrol.ThesefindingssuggesttheexistenceoftheIgEmemoryBcellsinthemiceaftertheprimaryTCSimmunization.

简介：Asimplemethodtocreateachromosome-specificDNAlibrqaryofrice,includingmicrodissection,amplification,charterizationandcloning,isdescribed.Ricechromosome4fromametaphasecellhasbeenisolatedandamplifiedbytheLinkerAdapterPCR(LA-PCR).ThePCRproductswerelabeledasprobeswithDIG-11-dUTPusingtherandomprimingmethod.SouthernblotanalysiswithricegenomicDNAandspecificRFLPmarkersdemonstratedthatthePCRproductswerederivedfromricechromosome4.Alargelibrarycomprisingover100,000recombinantplasmidmicroclonesfromricechromosome4wasconstructed.Colonyhybridizationshowedthat58%oftheclonescontainedsingleorlow-copysequencesand42%containedrepetitivesequences.ThesizeofinsertsgeneratedbyPCRrangedfrom140bpto500bp.ThismethodwillfacilitatecloningofthespecificchromosomeDNAmarkersandimportantgenesofrice.

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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。

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简介：Interleukin-4isacytokineproducedbyactivatedTcells,mastcells,andbasophilsthatelicitsmanyimportantbiologicalresponses[1](seeTab1).TheseresponsesrangefromtheregulationofhelperTcelldifferentiation[2]andtheproductionofIgE[3]totheregulationoftheadhesivepropertiesofendothelialcellsviaVCAM-1[4],Inkeepingwiththesediversebiologicaleffects,high-affinitybindingsitesforIL-4(Kd20to300pM)havebeendetectedonmanyhematopoieticandnon-hematopoieticcelltypesatlevelsrangingfrom50to5000sitespercell[5].ThisreviewwillfocusonthediscretesignaltransductionpathwaysactivatedbytheIL-4recxeptorandthecoordinationoftheseindividualpathwaysintheregulationofafinalbiologicaloutcome.

简介：Hybridoma房间在抗体生产率追随者暴露显示增加到张力亢进的条件。然而，内在的机制很好没被理解。在现在的学习，我们假设激活的T房间的原子因素5(NFAT5)/tonicityenhancer绑定蛋白质(TonEBP)工作增加hybridomacells的抗体生产率。NFAT5是osmosensitive哺乳动物的抄写因素。然而，它在没在张力亢进的周围被洗的各种各样的器官的无所不在的表示建议NFAT5可以也在等渗的条件下面调整细胞生长和功能。在这研究，我们由西方的污点分析在hybridoma房间检验了表示ofNFAT5，并且发现它在张力亢进的媒介显著地增加了。为了推进，在hybridoma房间定义NFAT5的功能，RNA干扰技术习惯于down在SGB-8房间(一根hybridoma房间线)调整NFAT5的表示。在等渗的媒介，hybridoma房间的抗体生产率被NFAT5while的down规定减少细胞增殖没被影响。这里介绍的结果表明那NFAT5不仅在hybridoma房间在渗透的压力反应小径起一个重要作用而且为最佳的抗体生产率是必要的。

简介：Perforin是主要从事调停的形成毛孔的蛋白质目标T房间死亡并且被细胞毒素的T淋巴细胞(CTL)和自然漂亮房间采用。然而，它是否也在常规CD4+T房间功能起一个作用，仍然保持不清楚。这里，我们报导那在perforin缺乏(PKO)老鼠，CD4+T房间是响应T的hyperproliferative房间受体(TCR)刺激。hyperproliferation的这个特征被改进在房间分割并且在IL-2分泌物伴随。看起来，perforin缺乏不在胸腺怒气和淋巴节点影响T房间开发。在vivo，perforin缺乏导致增加的抗原特定的T房间增长和抗体生产。而且，PKO老鼠更产生试验性的自体免疫的眼色素层炎。探讨分子的机制，我们发现在TCR刺激以后，从PKO老鼠的CD4+T房间显示增加的细胞内部的钙流动并且随后提高抄写因素NFAT1的激活。我们的结果显示perforin在由影响TCR依赖的Ca2+发信号调整CD4+T房间激活和有免疫力的反应起一个否定作用。

简介：在脂肪和肌肉房间，刺激胰岛素的葡萄糖举起被葡萄糖transporter主要调停4(GLUT4)，哪个到响应胰岛素刺激的房间表面的从细胞内部的分隔空间的translocates。AS160是Akt的底层之一并且在调整胰岛素的GLUT4translocation起重要作用。在这研究，(RUVBL2)象RuvB一样蛋白质2用与集体spectrometry相结合的哺乳动物的双人脚踏车亲密关系纯化(龙头)作为新AS160有约束力的蛋白质被识别。在3T3-L1adipocytes，RUVBL2高度被表示并且在cytosol主要是分布式的。在adipocytes的RUVBL2的弄空通过减少刺激胰岛素的AS160phosphorylation禁止刺激胰岛素的GLUT4translocation和葡萄糖举起。然而，人的RUVBL2的介绍能颠倒这禁止的效果。这些数据建议RUVBL2通过它和AS160的相互作用在刺激胰岛素的GLUT4translocation起一个重要作用。

简介：POU抄写因素OCT4不仅在维持pluripotent和房间而且幕作为通过基因剂量的一个房间命运决定因素完成的胚胎的茎(ES)的自我更新的状态起一个必要作用。然而，控制细胞内部的OCT4蛋白质水平的分子的机制留下逃犯。这里，我们报导那人的WWP2，E3ubiquitin(Ub)蛋白质ligase，通过它的WW领域明确地与OCT4交往并且在vitro并且在vivo提高OCT4的Ub修正。我们首先证明在人的ES房间的内长的OCT4能被Ubpost-translationally修改。而且，我们发现WWP2以一种剂量依赖者方式，和WWP2的活跃地点半胱氨酸残余通过26Sproteasome支持了OCT4的降级在OCT4上为它的酶的活动和解朊的效果被要求。显著地，我们当WWP2表示是由特定的RNA干扰(RNAi)的downregulated时，内长的OCT4蛋白质水平显著地被提高的数据表演，建议那WWP2是为在人的ES房间维持合适的OCT4蛋白质水平的一个重要管理者。而且，北污点分析证明WWP2抄本在多样的人的织物/器官是广泛地在场的并且高度在无差别的人的ES房间表示了。然而，它的表示水平快速在区分的人的ES房间以后被减少，显示WWP2表示力量发展地被调整。我们的调查结果证明WWP2是在人的ES房间的OCT4蛋白质水平的一个重要管理者。

简介：IL-16isaligandandchemotacticfactorforCD4+Tcells.IL-16inhibitstheCD3mediatedlymphocyteactivationandproliferation.TheeffectsofIL-16onthetargetcellsaredependentonthecelltype,thepresenceofco-activatorsetc.TounderstandtheregulationfunctionandmechanismofIL-16ontargetcells,weuseda130a.a.recombinantIL-16tostudyitseffectsonthegrowthofJurkatTleukemiacellsinvitro.WefoundthattherIL-16stimulatedtheproliferationofJurkatcellsatlowdose(10^-9M),butinhibitedthegrowthofthecellsathigherconcentration(10^-5M).Resultsshowedthat10^-5MofrIL-16treatmentinducedanenhancedapoptosisinJurkatcells.ThetreatmentblockedtheexpressionofFasL,butup-regulatedthec-mycandBidexpressioninthecells.Pre-treatmentofPKCinhibitororMEK1inhibitormarkedlyincreasedordecreasedtherIL-16inducedgrowth-inhibitingeffectsonJurkatcells,respectively.TheresultssuggestedthattherIL-16mightbearegulatorforthegrowthorapoptosisofJurkatcellsatadose-dependentmanner.Thegrowth-inhibitingeffectsofrIL-16mightbeFas/FasLindependent,but,associatedwiththeactivationofPKC,up-regulatedexpressionofc-MycandBid,andtheparticipationoftheERKsignalpathwayinJurkatcells.

简介：Thenuclearmatrixattachmentregions(MARs)andthebindingnuclearmatrixproteinsinthe5'-flankingcisactingelementsofthehumanε-globingenehavebeenexamined.UsinginvitroDNA-matrixbindingassay,ithasbeenshownthatthepositivestage-specificregulatoryelement(ε-PREII,-446bp--419bp)upstreamofthisgenecouldspecificallyassociatewiththenuclearmatrixfromK562cells,indicatingthatε-PREIImaybeanerythroidspecificfacultativeMAR.IngelmobilityshiftassayandSouthwesternblottingassay,anerythroid-specificnuclearmatrixprotein(ε-NMPk)inK562cellshasbeenrevealedtobindtothispositiveregulatoryelement(ε-PREII).Furthermore,wedemonstratedthatthesilencer(-392bp--177bp)upstreamofthehumanε-globingenecouldassociatewiththenuclearmatricesfromK562,HELandRajicells.Inaddition,thenuclearmatrixproteinspreparedfromthesethreecelllinescouldalsobindtothissilencer,suggestingthatthissilencerelementmightbeaconstitutivenuclearmatrixattachmentregion(constitutiveMAR).Ourresultsdemonstratedthatthenuclearmatrixandnuclearmatrixproteinsmightplayanimportantroleintheregulationofthehumanε-globingeneexpression.