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

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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：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：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.

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简介：Glatiramer醋酸盐(GA)是过去常对待多重硬化的immunomodulatory肽药。它的处理效果被扩展了到象uveoretinitis，煽动性的肠疾病，接枝拒绝和肝的纤维变性那样的另外的自体免疫的条件。这里，我们报导GA在在cyclophosphamide(CY)改变糖尿病的临床的功课是有效的加强的非肥胖的糖尿病患者(CY点头)老鼠。有显著地减少的GA的治疗在老鼠和改善insulitis的糖尿病的率，它与增加的CD4+CD25+Foxp3+T房间反应与一致在对待老鼠。GA处理导致了抄写因素Foxp3的增加的表示并且在vivo并且在vitro提高了interleukin-4(IL-4)的生产。Foxp3的起来规定上的GA的效果通过IL-4部分被调停，是明显的。IL-4被发现维持Foxp3表示和CD4+CD25+规章的T房间(Tregs)的规章的功能。这研究提供GA通过Tregs的正式就职为类型1糖尿病有处理潜力，那增加的IL-4生产为提高的Treg在GA处理的功能部分负责的新证据。

简介：MCM10蛋白质是涉及DNA的开始的一个必要复制因素。开始发育的酵母的mcm10异种(mcm10-1)在37度C显示出生长拘捕。在现在的工作，我们孤立mcm10-1压制或拉紧，它在37度C成长。有趣地，这mcm10-1压制或在14度C经历房间周期拘捕。新奇基因，YLR003c，被这的高拷贝的互补识别压制或。我们作为Cms1(看10Suppressor的互补)叫了它。而且，转变的实验证明mcm10-1的房间压制或在14度C与高拷贝的原生质标志然而并非低拷贝的原生质标志成长，在Cms1的表示上显示那能救这mcm10的生长拘捕压制或在非容许的温度。这些结果建议那CMS1蛋白质可以机能上地与MCM10蛋白质交往并且在DNA和房间周期控制的规定起一个作用。

简介：Glucosetransporter4(GLUT4)isresponsibleforinsulin-stimulatedglucosetransportingintotheinsulin-sensitivefatandmusclecells.ThedynamicsofGLUT4storagevesicles(GSVs)remainstobeexploredanditisunclearhowGSVsarearrangedbasedontheirmobility.Weexaminedthisissuein3T3-L1cellsviainvestigatingthethree-dimensionalmobilityofsingleGSVlabeledwithEGFP-fusedGLUT4.Athinlayerofcytosolrightadjacenttotheplasmamembranewasilluminatedandsuccessivelyimagedat5Hzunderatotalinternalreflectionfluorescencemicroscopewithapenetrationdepthof136nm.Employingsingleparticletracking,thethree-dimensionalsubpixeldisplacementofsingleGSVwastrackedataspatialprecisionof22nm.Boththemeansquaredisplacementandthediffusioncoefficientwerecalculatedforeachvesicle.Trackingresultsrevealedthatvesiclesmovedasifrestrictedwithinacagethathasameanradiusof160nm,suggestingthepresenceofsomeintracellulartetheringmatrix.ByconstructingthehistogramofthediffusioncoefficientsofGSVs,weobservedasmoothdistributioninsteadoftheexistenceofdistinctgroups.TheresultindicatesthatGSVsaredynamicallyretainedinacontinuousandwiderangeofmobilityratherthanintoseparateclasses.

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