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

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

简介：hPFTAIRE1(PFTK1)，Cdc2相关的蛋白质kinase，高度在人的大脑被表示。它在Hela房间展出细胞质的分发，尽管它在它的N终点包含二个原子本地化信号(NLS)。到为它的底层和规章的部件的搜索，我们由把全身的hPFTAIRE1用作一个诱饵屏蔽了一个二混血儿的图书馆。四14-3-3isoforms(贝它，epsilon，希腊语字母的第七字，字形物)被识别与hPFTAIRE1交往。我们在hPFTAIRE1发现了一个通常认为的14-3-3绑定一致主题(RHSSPSS)，它与它的第二NLS重叠了。RHSSPSS主题的删除或有在保存有约束力的主题的翼的Ser119的替换废除了在hPFTAIRE1和14-3-3蛋白质之间的特定的相互作用。变异的S120AhPFTAIRE1也显示出一个弱相互作用到14-3-3蛋白质。结果建议Ser119为在hPFTAIRE1和14-3-3蛋白质之间的相互作用是关键的。当熔化了到绿荧光灯的蛋白质(GFP)的C终点时，所有hPFTAIRE1异种在Hela房间和人的neuroblastoma房间(SH-SY5Y)的细胞质散布了，显示有14-3-3蛋白质的那绑定不贡献潜水艇hPFTAIRE1的细胞的本地化，尽管绑定可以涉及它的发信号的规定。

简介：Thenon-classicalHLAclassIantigenHLA-GisanimmunemodulatorwhichinhibitsthefunctionsofTcells,NKcells,andtheDendriticcells(DC).Asaresult,HLA-Gexpressioninmalignantcellsmayprovidethemwithamechanismtoescapetheimmunesurveillance.Inmelanoma,HLA-Gantigenexpressionhasbeenfoundin30%ofsurgicallyremovedlesionsbutinlessthan1%ofestablishedcelllines.OnepossiblemechanismunderlyingthedifferentialHLAGexpressioninvivoandinvitroisthattheHLA-Ggeneisepigeneticallyrepressedinmelanomacellsinvitro.Totestthishypothesis,wetreatedtheHLA-GnegativemelanomacelllineOCM-1AwiththeDNAmethyltransferaseinhibitor5-aza-2'-deoxycytidine(5-AC)andanalyzedwhetherHLA-Gexpressioncanberestored.OurdatastronglysuggestthatHLA-GissilencedasaresultofCpGhypermethylationwithina5'regulatoryregionencompassing220bpupstreamofthestartcodon.Aftertreatment,HLA-GmRNAexpressionwasdramaticallyincreased.WesternblotandflowcytometryshowedthatHLA-Gproteinwasinduced.Interestingly,HLA-Gcellsurfaceexpressiononthe5-ACtreatedOCM-1AcellsismuchlessthanthatontheHLA-GpositiveJEG-3cellswhileasimilaramountoftotalHLA-Gwasobserved.Possiblemechanismsforthedifferencewereanalyzedinthestudysuchascellcold-treatment,peptideloadingandantigenprocessingmachinerycomponents(APM)aswellasβ2microglobulin(β2-m)expression.DatarevealedthattheAPMcomponentcalreticulinmightbeinvolvedinthelowerHLA-GsurfaceexpressiononOCM-1Acells.Takentogether,ourresultsindicatedthatDNAmethylationisanimportantepigeneticmechanismbywhichHLA-Gantigenexpressionismodulatedinmelanomacellsinvitro.Furthermore,tothefirsttime,wehypothesizedthatthedeficiencyofcalreticulinmightbeinvolvedinthelowHLA-Gsurfaceexpressiononthe5-ACtreatedOCM-lAcells.

简介：<正>Uponactivation,naiveT-helpercellscandifferentiateintotwomajordistinctsubsets,Thelper1(Th1)andThelper2(Th2),asdefinedbytheireffectorfunctionsandcytokinesecretionpatterns.CytokinemilieuandcostimulatorymoleculeshavebeenshowntoplayanessentialroleindeterminingThelperdifferentiation.However,itisstillunclearhowtheeffectsofsignalsofco-stimulatorymoleculesandcytokinesareexertedduringThelperdifferentiation.Weshowevidencesuggestingthatwhilecytokinesignalsinitiatedifferentiationprogram,theselectiveactionofdeatheffectorsdeterminestheendpointbalanceofdifferenti-

简介：目的通过观察左归丸含药血清对成骨细胞白细胞介素-1（IL-1）、白细胞介素．6（IL-6）和环加氧酶-2（COX-2）表达的影响，探讨其治疗骨质疏松症的作用机制。方法体外分离、培养成骨细胞，实验分为3组：正常血清组、卵巢切除（OVX）血清组和OVX含药血清组。采用免疫组化法，检测成骨细胞IL-1、IL-6和COX-2的表达。结果OVX血清组成骨细胞IL-1、IL-6和COX-2的表达明显强于正常血清组，而OVX含药血清组的表达较OVX血清组明显减弱，与正常血清组比较，则无显著性差异。结论在去势状态下，左归丸可能是通过抑制成骨细胞IL-1、IL-6和前列腺素E2（PGE2）的分泌，进而达到治疗骨质疏松的作用。

简介：Amurinemacrophage-likecelllineJ774,acquired,inresponsetoLPS,anabilitytokilltumornecrosisfactor(TNF)-insensitivetargetP815mastocytomacellswhereasanothercellline,P388D1didnot,LPStriggeredsignalingmechanismsbetweenthetwocelllineswerecomparedwithanaimtoinquireaboutthepossiblenatureoftheabove-mentioneddifference,TheresultswhowedthattwocelllinesrespondtoLPS-treatmentbyparallelactivationofbothphospholipasesCandA2(PLCandPLA2)toapproximatelythesameextent.ThemaximumresponseoftothenzymesofJ774cellswasnotedwithin10minthetreatmentwhereasthatofP388D1cellsrequiredmorethan20min,TheotherpropertiesofLPS-responsiveenzymesstudiedweresimilarbetweentwocelllines,includingActivationofPLCandPLA2andPKCinmacrophagesbyLPS.Ca2+augmentationofenzymeactivation,participationofguaninenucleotidebinding(G)proteinsintheinitialactivationpreocesses,andinhibitionofenzymeactivationbythepriortreatmentofcellswithcholeraorpertussistoxinsetc.Moreover,LPS-triggeredactivationofPLCandPLA2wasfoundtobefollowedbytheincreaseofPKCactivitiesinbothcelllines.Inspiteofthesesimilarities.J774cellspossessedbothbasicandacidicformsofPKCactivities,whileP388D1cellsownedonlyPKCofbasicform,Nevertheless,thequestionwhyJ774cellsbutnotP388D1cells,canacquirethetumoricidalactivity,aganistP815,cellsfollowingLPStreatmentrematinstobeanswered.

简介：Amurinemacrophage-likecellline,J774,acquried,inresponsetoLPS,anabilitytokilltumornecrosisfactor（TNF）-insensitivetargetP815mastocytomacells,whereasanothercellline,P388D1,didnot.LPS-triggeredsignalingmechanismsbetweenthetwocelllineswerecomparedwithanaimtoinquireaboutthepossiblenatureoftheabove-mentioneddifference.TheresultsshowedthattwocelllinesrespondtoLPS-treatmentbyparallelactivationofbothphospholipasesCandA2（PLCandPLA2）toapproximatelythesameextent.ThemaximumresponseofbothenzymesofJ774cellswasnotedwithin10minofthetreatment,whereasthatofP388D1cellsrequiredmorethan20min.TheotherpropertiesofLPS-responsiveenzymesstudiedweresimilarbetweentwocelllines,ineludingActivationofPLCandPLA2andPKCinmacrophagesbyLPSCa2+augmentationofenzymeactivation,participationofguaninenucleotidebinding（G）proteinsintheinitialactivationprocesses,andinhibitionofenzymeactivationbythepriortreatmentofcellswithcholeraorpartussistoxinsetc.Moreover,LPS-triggeredactivationofPLCandPLA2wasfoundtobefollowedbytheincreaseofPKCactivitiesinbothcelllines.Inspiteofthesesimilarities,J774cellspossessedbothbasicandacidicformsofPKCactivities,whileP388D1cellsownedonlyPKCofbasicform.Nevertheless,thequestionwhyJ774cells,butnotP388D1cells,canacquirethetumoricidalactiyity,aganistP815cellsfollowingLPS-treatmentremainstobeanswered.

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：Bcl-2基因属于Bcl-2基因家族，其表达的Bcl-2蛋白在细胞凋亡过程中通过抑制线粒体中细胞色素C的释放，可明显地抑制细胞凋亡。由于在大规模的细胞培养过程中，细胞的死亡以凋亡为主，所以可通过建立稳定过表达Bcl-2蛋白的重组细胞株，以抑制细胞的凋亡。同时，Bcl-2蛋白的变化不但可预见肿瘤的发生，而且通过药物降低Bcl-2的含量对于肿瘤的治疗也具有积极的意义。本文综述了Bcl-2蛋白的结构、功能、抗凋亡作用的机理，以及目前在生物制药和临床方面的应用和前景。

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

简介：Arabidopsisthaliana嘘一deacetylase1(AtHD1或AtHDA19)，酵母RPD3的一个相当或相同的事物，是在植物的许多生理、发展的过程的一个全球管理者。尽管有为在植物基因规定和开发的AtHD1的一个角色的基因证据，AtHD1的生物化学、细胞的性质糟糕被理解。这里，我们在vivo报导AtHD1的细胞的本地化模式并且嘘在vitro的一项deacetylase活动。绿荧光灯的蛋白质(GFP)的短暂、稳定的表示在洋葱房间标注了AtHD1并且分别地，在转基因的Arabidopsis的根，种子和叶子表明AtHD1在euchromatic区域大概在原子核是局部性的并且从核排除。AtHD1的本地化模式与涉及核形成和transgenes的silencing并且分别地重复了DNA元素的AtHD2和AtHDA6的那些不同。另外，一hist一deacetylase活动试金证明在细菌生产的recombinantAtHD1示威了一特定嘘在vitro的一项deacetylase活动。数据建议AtHD1是原子蛋白质并且拥有嘘为对植物生长和开发重要的全球transcriptional规定负责的一项deacetylase活动。

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：1资料与方法1.1临床资料患者女．26岁．因躯干部皮损逐渐增多半年，于2004年12月5日来本院就诊。半年前患者发现躯干部出现点状红褐色皮损，微痒．未予诊治．之后皮损逐渐增多。发病以来，患者饮食、睡眠可．二便如常。既往体健．无家族史。体格检查：躯干部皮肤散在性分布多数与毛囊一致的红褐色扁平丘疹，直径于0.5cm左右．有光泽．细屑不明显：

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简介：用原子力显微镜（AFM）观察线性DNA并探讨其成像条件。用RT-PCR技术扩增柯萨奇B1病毒VP1基因DNA片段，纯化回收后配制成含和不含1mmol/LMgCl2的水溶液，DNA终浓度为100μg/ml。分别取20μl滴加在新鲜解理的云母片上，吸收1min，用滤纸吸去残液，氮气吹干，在室温下采用MultiModeAFMNanoscopeⅢa的敲击模式成像。同时比较新制备和多次使用过的探析所获得图像的质量，对两种探针进行扫描电镜观察。电泳证明获得了0.83kb的VP1基因DNA线性片段，Mg^2+存在时，DNA在云母片上吸附延展较好，所获图像质量优于无Mg^2+时。新制备的探针较多次使用过的探针所获图像分辨率更高。DNA分子的表现宽度为18±2.9nm，高度为0.8±0.2nm。说明AFM能以高分辨率直接观察DNA分子，Mg^2+的存在和高质量的探针有助于获得理想的图象。

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