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简介：死亡联系域的蛋白质Daxx施加包括调停的许多报导功能经由激活c6月N终端从FasL发信号到apoptosisapoptosis的kinase(JNK)，正式就职和抑制，和染色质改变的规定。它原来从酵母被克隆用船边交货对相似物体之连续感觉而形成心像口的细胞内部的尾巴的二混血儿的屏幕诱饵。而许多起始的报告仍然保持争论，Daxx在一系列压力信号包括UVirradiation，过氧化氢治疗和TGF-β治疗触发的apoptosis的规定起重要作用，是清楚的。在这评论，我们在Axinbeing上集中连接Daxx到p53的一个拴住的因素。

简介：CCAAT/enhancer有约束力的蛋白质α(C/EBPα)是transcriptional禁止细胞增殖的规章的因素，和其他的翻译开始生产二多肽，C/EBPαp30并且C/EBPαp42。由表示介绍，C/EBPαp30specifically禁止了基因的一个唯一的集合，这被揭示，包括MPP11，p84N5和SMYD2，它没被C/EBPαp影响42在两根QSG-7701hepatocyte房间线和QGY-7703hepatoma，cells.Semi量的RT-PCR分析独立地证实了这些结果。Chromatinimmunoprecipitation试金显示出30比C/EBPαp更强烈绑了在这些基因的倡导者的那C/EBPαp42。在C/EBPα是调整的down的临床的hepatoma在样品，所有三基因明确地由30在上面的C/EBPαp禁止了调整。然而，MPP11，p84N5和SMYD2genes的压抑可能直接不涉及C/EBPαp30-mediated生长抑制。我们的数据建议30调整的那C/EBPαp目标基因的一个唯一的集合并且多于C/EBPαp的dominant-negativeregulator42。

简介：CD4T助手(Th)房间在适应有免疫力的回答起关键作用。他们包括B房间，CD8T房间，巨噬细胞，桅杆房间，neutrophils，嗜曙红血球和basophils招募并且激活另外的有免疫力的房间。基于他们的功能，他们cytokine分泌物的模式和他们特定的抄写因素的表示，Th房间，区分开来与na?veCD4T房间，被分类进四个主要的系，Th1，Th2，Th17和T规章(Treg)房间，尽管另外的Th系可以存在。一样的系的子集可以表示不同受动器cytokines，在不同地点住或而从不同的系的房间可以分泌普通cytokines，产生有不同命运的房间，导致Th房间人口的巨大的异质，例如IL-2，IL-9和IL-10。另外，cytokine分泌物的模式可以在某些情形下面向另外一个从一个系的切换，建议Th房间是塑料的。Tregs比原来是思维的也更异构、塑料。在这评论，我们在Th房间的异质和粘性上总结最近的报告，并且讨论如此的特征的潜在的机制和Th房间显示的含意。

简介：ApoptosisplaysanessentialroleinTcellbiology.ThymocytesexpressingnonfunctionalorautoreactiveTCRsareeliminatedbyapoptosisduringdevelopment.ApoptosisalsoleadstothedeletionofexpandedeffectorTcellsduringimmuneresponses.Thedysregulationofapoptosisintheimmunesystemresultsinautoimmunity,tumorogenesisandimmunodeficiency.Twomajorpathwaysleadtoapoptosis:theintrinsiccelldeathpathwaycontrolledbyBcl-2familymembersandtheextrinsiccelldeathpathwaycontrolledbydeathreceptorsignaling.Thesetwopathwaysworktogethertoregu

简介：在Saccharomycescerevisiae，必要基因CDC13编码telomeric遗传上并且身体上与Stn1p和Ten1p交往的搁浅单人赛的DNA有约束力的蛋白质，并且为telomere结束保护和telomere长度控制被要求。Ten1由参予telomere长度规定和染色体结束保护的分子的机制留下逃犯。在这个工作，我们用净化的recombinantCdc13p和Ten1p在胶化过滤分析观察了Cdc13p和Ten1p的一个弱相互作用。Ten1p本身展出一项弱DNA有约束力的活动，但是提高telomericTG1鈥吗？Cdc13p的DNA有约束力的能力。Cdc13p是有Ten1p的co-immunoprecipitated。在变异的ten1-55或ten1-66房间，在Ten1p和Cdc13p之间的损害相互作用与telomericDNA导致长得多的telomeres，以及Cdc13p的一个减少的协会。一致地，Ten1-55和Ten1-66异种蛋白质没能刺激telomeric在vitro的Cdc13p的DNA有约束力的活动。这些结果建议Ten1p提高telomericCdc13p到的DNA有约束力的活动否定地调整telomere长度。

简介：Immunotherapythatspecificallytargetstumorcellsisthepreferredapproachtoinducetumorregression.Overthepastdecade,significantprogresshasbeenmadeindevisingvariousmethodstodirecttheimmunesystemtorespondtotumorcells.Themajorhurdleforsuccessfulimmunotherapyistoovercomeimmunetoleranceinthetumormicroenvironment.Recentclinicaltrialswithdendriticcell-basedvaccination[1,2]andCTLA4blockingantibodies[3]haveshowngreatpromise,thoughcompletecancerregressionisnotalwaysachieved[4].Currently,alternativestrategiespotentiallyleadingtocancereradicationorregressioninanimalorclinicalmodelsarebeingenthusiasticallypursued.InthisissueofCellResearch,Wangetal.reportanovelwaytoinducetumorimmunitybytheuseofirradiatedautologousTcells[5].

简介：TheundecapeptidesubstanceP(SP)wasshowntobeintimatelyinvolvedinboththestructuralandfunctionalaspectsoftheanteriorpituitary.Yet,inadditiontoitsinfluencesonhormonalsecretion,SPmaywellpossessmoreactionsinthismastergland.ThepresentstudywasfthereforeaimedtoinvestigatetheeffectofSPontheproliferationofratanteriorpituitarycellsinprimaryculture,ItwasfoundthatSPcoulddose-dependentlyincreasetheincorporationoftritiatedthymidine(3H-TdR)intoculturedanteriorpituitarycells.OthermammaliantachykininssuchasneurokininAandneurokininBhadsimilareffectbuttovaryingdegrees.TheequipotentanalogueofSP,Norleucine^11-SP(Nle^11-SP),alsoactedlikewise.withitsactionantagonizablebyspantide,aSPreceptorblocker.TofurthercharacterizethenatureofcellsresponsivetothechallengeofSP,immunocytochemicalstainingagainstS-100proteinandsomeadenohypophysealhormoneswasperformedaloneorplusautoradiography.TheresultsshowedthatthepercentageofS-100proteinimmunorectivecellswasapparentlyelevatedbytheaddtionofNle^11-Spfor48h,whichindicatesapreferentialproliferationoffolliculo-stellatecellsundertheregime.ThiswasconfirmedbyincreasesinimmunocytochemicalorautoradiographicallabellingindicesofanteriorpituitarySubstancePandanteriorpituitarycellproliferation.Cellstreatedsimilarly.Takentogether,TheseresultsrevealthatthetrophicactionofSPobservedpreviouslyinothertissuesisalsopresentatleastinculturedratanteriorpituitarycells.withrespondingcellsbeingpredominantlyfolliculo-stellatecellsastypifiedbyS-100proteinimmunoreactivity.Therefore,anintra-pituitarytrophicactionofSPinvivocouldbeanticipated.

简介：cAMPmediatedsignalingmayplayasuppressiveroleinimmuneresponse.WepreviouslyfoundthatthecAMP-elevators(CTxand8-Br-cAMP)inhibitedIL-12,IL-la,IL-6geneexpression,butincreasedthetranscriptionallevelsofIL-10andIL-1RainLPS-treatedmurineperitonealmacrophages.ThepresentstudyexaminedapossiblemolecularmechanisminvolvedincAMPelevators-inducedinhibitionofIL-12p40expressioninresponsetoLPS.OurdatademonstratedthatcAMPelevatorsdownregulatedIL-12p40mRNAexpressionandIL-12pT0productioninmurineperitonealmacrophages.SubsequentstudiesrevealedthatcAMP-elevatorsblockedphosphorylationofp38MAPK,butdidnotaffecttheactivityofNF-κBbindingtoIL-12promoter(-136/-112).ThisisthefirstreportthatcAMPelevatorsinhibitLPS-inducedIL-12productionbyamechanismthatisassociated,atleastinpart,withp38-dependentinhibitionbycAMPsignalingpathways.

简介：Granulocyte巨噬细胞刺激殖民地的因素(GM-CSF)是一个重要造血的生长因素和有免疫力的调节的人。GM-CSF也在各种各样的传播白血球的功能的活动有深刻效果。它被许多房间类型在收到有免疫力的刺激之上包括T房间，巨噬细胞，endothelial房间和成纤维细胞生产。尽管GM-CSF局部地被生产，它能以一种paracrine方式行动到在主人防卫提高他们的功能的成员传播neutrophils，单核白血球和淋巴细胞。最近的集中的调查为它增加树枝状的房间(DC)成熟和功能以及巨噬细胞活动的能力作为一个有免疫力的助手在GM-CSF的应用程序上被集中。在经历化疗的癌症病人对待嗜中性白血球减少症临床上被使用，在在治疗期间的爱滋病病人，并且在在骨髓移植以后的病人。有趣地，GM-CSF-deficient老鼠的造血的系统看起来正常；最重要的变化在一些特定的T房间回答。尽管GM-CSF的分子的克隆用T房间的cDNA图书馆被执行，T房间在激活以后生产GM-CSF，是众所周知的，在T房间功能上有在由T房间和它的效果的生产的这cytokine的系统的调查的缺乏。在这篇文章，我们将在T房间主要集中于GM-CSF的免疫生物学。

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简介：TherearetwopossibleoutcomeswhenDNAdamageoccursinnormalmammaliancells:eitherinductionofcell-cyclecheckpointwhichinhibitstheprogressofthecellcyclesaswellasactivatesDNArepairpathways,oractivationofapoptosistoeliminatedamagedcells.Thep53tumour-suppressorgeneplaysakeyroleinselectingthesepathways.Inourpresentworks,thehumangastriccancercelllineAGSwastreatedwithtripchlorolide,apotentantitumorcompoundpurifiedfromaChineseherbTripterygiumWilfordiiHook.Singlecellgelelectrophoresis(Cometassay)showedthatthetreatmentoftripchlorolideresultedinDNAdamageinAGScells.ThedamagedAGScellswentthroughapoptosis,whichwastime-anddose-dependent.

简介：Recentstudiesindicatethatcell-cyclecheckpointsaretightlycorrelatedwiththeregulationofapoptosis,inwhichp53playsanimportantrole.OurpresentworksshowthattheexpressionofE6/E7oncogenesofhumanpapillomavirusinHeLacellsisinhibitedinthepresenceofanti-tumorreagenttripchlorolide(TC),whichresultsintheup-regulationofp53inHeLacells.Interestingly,underthesameTC-treatment,thecellsattheearlyS-phasearemoresusceptibletoapoptosisthanthoseatthemiddleS-phasealthoughp53proteinisstabilizedtothesamelevelinbothsituations.Significantdifferenceisexhibitedbetweenthetwospecifiedexpressionprofiles.Furtheranalysisdemonstratesthatanti-apoptoticgenesurvivinisup-regulatedbyp53intheTC-treatedmiddle-Scells,whereasitisdown-regulatedbyp53intheTC-treatedearly-Scells.Takentogether,thepresentstudyindicatesthatthedifferentialp53-regulatedexpressionofsurvivinatdifferentstagesofthecellcycleresultsindifferentcellularoutputsunderthesameapoptosis-inducer.

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简介：CREB有约束力的蛋白质(CBP)和它的相当或相同事物p300是涉及细胞的活动的一个宽数组的各种各样的顺序特定的抄写因素的transcriptionalco使活跃之物，例如脱氧核糖核酸修理，房间生长，区别和apoptosis。Severalstudies建议了CBP和p300可能被看作瘤压制ors，与他们是的突出的角色响应各种各样的刺激的不同基因表示模式的跨coupling。他们主要经由乙酰化施加行动嘘和另外的规章的蛋白质(例如p53)。在CBP/p300功能的主要悖论是他们似乎能够贡献各种各样的反对细胞的进程。呼吸上皮tumorigenesis代表一个范围的多步累积的一个复杂过程基因并且epigenetic错误。通过激活和压抑的建筑群的交替的形成的Transcriptionmodulation是这些精神错乱的最终的收敛点，并且CBP/p300在这相互影响代表关键参加者。因此，他们的分子的行动和相互作用的照明能在呼吸上皮carcinogenesis为药理学干预揭示新潜在的目标。

简介：Changesinthedistributionof1P1-antigeninthedevelopingchickretinahavebeenexaminedbyindriectimmunofluorescencestainingtechniqueusingthenovelmonoclonalantibody(MAb)1P1.Expressionofthe1P1antigenwasfoundtoberegulatedinradialaswellasintangentialdimensionoftheretina,beingpreferentiallyorexclusivelylocatedintheinnerandouterplexiformlayersoftheneuralretinadependingonthestagesofdevelopment,Withtheonsetoftheformationoftheinnerplexiformlayer1P1antigenbecomesexpressedintheretina.Withprogressingdifferentiationoftheinnerplexiformlayer1P1immunofluorescencerevealed2subbandsatE9and6subandsatE18,Atpostnatalstages(afterP3)immunoreactivitywasreducedinaninside-outsidesequenceleadingtothecompleteabsenceofthe1P1antigeninadulthood.1P1antigenexpressionintheouterplexiformlayerwasalsosubjecttodevelopmentalregulation.Thespation-temporalpatternof1P1antigenexpressionwascorrelatedwiththetimecourseofhistologicaldifferentationofchickretina,namelythesynapserichplexiformlayers.Whetherthe1P1antigenwasfunctionallyinvolvedindendriteextensionandsynapseformationwasdiscussed.

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