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:AninteractivetooltovisualizetheK-stringcompositionoflongDNAsequencesincludingbacterialcompletegenomesisdescribed.Itisespeciallyusefulforexploringshortpalindromicstructuresinthesequences.TheSeeDNAprogramrunsonRedHatLinuxwithGTK+support.Itdisplaystwo-dimensional(2D)orone-dimensional(1D)histogramsoftheK-stringdistributionofagivensequenceand/oritsrandomizedcounterpart.ItisalsocapableofshowingthedifferenceofK-stringdistributionsbetweentwosequences.TheCsourcecodeusingtheGTK+packageisfreelyavailable.
简介:目的:构建4E—BPl及其T37A、T46A、$65A、T70A突变体4E—BPl-4A基因表达的重组慢病毒载体,研究其对胃癌HGC27细胞生长的影响。方法:PCR扩增4E—BPl基因及其突变体aE—BPl-4A基因并克隆到pCDH载体,构建成pCDH-4E—BPl、pCDit一4E—BPl—4A,将其-9包装载体共转染293T细胞,包装成Lenti-4E—BPl及Lenti-4E—BPl—4A重组慢病毒载体,将此慢病毒感染胃癌HGC27细胞,Western印迹鉴定病毒载体介导的4E—BPl、4E~BPl—4A蛋白的表达,MTT、克隆形成和软琼脂方法研究过量表达4E—BPl、4E—BPl—4A对胃癌HGC27细胞生长的影响。结果:包装成Lenti-4E—BPl及Lenti-4E—BPl—4A重组慢病毒载体,并将此慢病毒载体感染胃癌HGC27细胞;MTT、克隆形成、软琼脂实验表明过量表达4E—BP!可抑制胃癌HGC27细胞的生长,过量表达4E—BP!一4A时抑制效果更明显。结论:构建了4E—BPl、4E—BPI-4A的重组慢病毒表达载体,在胃癌HGC27细胞中过量表达4E—BPl可抑制细胞生长,过量表达4E—BPl-4A的抑制效果更明显。
简介:Ionizingradiationisoneofthemosteffectivetoolsincancertherapy.Inapreviousstudy,wereportedthatproteintyrosinekinase(PTK)inhibitorsmodulatetheradiationresponsesinthehumanchronicmyelogenousleukemia(CML)celllineK562.Thereceptortyrosinekinaseinhibitor,genistein,delayedradiation-inducedcelldeath,whilenon-receptertyrosinekinaseinhibitor,herbimycinA(HMA)enhancesradiation-inducedapoptosis.Inthisstudy,wefocusedonthemodulationofradiation-inducedcelldeathbygenisteinandperformedPCR-selectsuppressionsubtractivehybridization(SSH)tounderstanditsmolecularmechanism.Weidentifiedhumanthymidinekinase1(TK1),whichiscellcycleregulatorygeneandconfirmedexpressionofTK1mRNAbyNorthernblotanalysis.ExpressionofTK1mRNAandTK1enzymaticactivitywereparallelintheirincreaseanddecrease.TK1isinvolvedinG1-Sphasetransitionofcellcycleprogression.Incellcycleanalysis,weshowedthatradiationinducedG2arrestinK562cellsbutitwasnotabletosustain.However,theadditionofgenisteintoirradiatedcellssustainedaprolongedG2arrestupto120h.Inaddition,theexpressionofcellcycle-relatedproteins,cyclinAandcyclinB1,providedtheevidencesofG1/SprogressionandG2-arrest,andtheirrelationshipwithTK1incellstreatedwithradiationandgenistein.TheseresultssuggestthattheactivationofTK1maybecriticaltomodulatetheradiation-inducedcelldeathandcellcycleprogressioninirradiatedK562cells.
简介:生节是对在昆虫的细菌的挑战的占优势的细胞的防卫反应。在这研究,Chrysomyamegacephala的第三个中间形态幼虫与细菌被注射,Escherichia关口iK12(106CFU/mL,2μL),立即在eicosanoid生合成的禁止者的注射以前,它严厉地减少的生节反应。测试幼虫与2(dexamethasone),cyclo-oxygenase(消炎痛,布洛芬和piroxicam),双cyclo-oxygenase/lipoxygenase(phenidone)和lipoxygenase(esculetin)和这些减少了的phospholipase的特定的禁止者被对待除了esculetin的生节。细菌的影响在注射(5nodules/larva)的2h以内是明显的,并且在8h以后增加了到最大值(与15nodules/larva),然后显著地减少了超过24h(9nodules/larva)。dexamethasone的禁止的影响在注射(4对5nodules/larva)的2h以内是明显的,并且生节显著地与控制相比被减少,在24h(5对8nodules/larva)上。布洛芬,消炎痛,piroxicam和phenidone的增加的剂量导致了小瘤的减少的数字。小瘤继续在蛹的阶段期间存在。然而,dexamethasone的效果被与eicosanoid先锋多元不堡和对待注射细菌的昆虫颠倒丰满的酸,arachidonic酸。这些调查结果同意了我们eicosanoid能调停的看法响应在另一Dipteran昆虫C的细菌的感染的细胞的防卫机制。megacephala。
简介:Mammaliancelltotipotencyisasubjectthathasfascinatedscientistsforgenerations.AlonglastingquestionwhethersomeofthesomaticcellsretainstotipotencywasansweredbythecloningofDollyattheendofthe20thcentury.Thedawnofthe218thasbroughtforwardgreatexpectationsinharnessingthepoweroftotipotentcyinmedicine.Throughstemcellbiology,itispossibletogenerateanypartsofthehumanbodybystemcellengineering.Considerableresourceswillbedevotedtoharnesstheuntappedpotentialsofstemcellsintheforeseeablefuturewhichmaytransformmedicineasweknowtoday.Atthemolecularlevel,totipotencyhasbeenlinkedtoasingulartranscriptionfactoranditsexpressionappearstodefinewhetheracellshouldbetotipotent.NamedOct4,itcanactivateorrepresstheexpressionofvariousgenes.Curiously,verylittleisknownaboutOct4beyonditsabilitytoregulategeneexpression.ThemechanismbywhichOct4specifiestotipotencyremainsentirelyunresolved.Inthisreview,wesummarizerethestructureandfunctionofOct4andaddresstoOct4functioninmaintainingtotipotencyorpluripotencyofembryonicstemcels.
简介:WehaverecentlyclonedapathogeninducibleblastresistancegenePi-khfromtheindicaricelineTetepusingapositionalcloningapproach.Inthisstudy,wecarriedoutstructuralorganizationanalysisofthePi-khlocusinbothindicaandjaponicaricelines.A100kbregioncontaining50kbupstreamand50kbdown-streamsequencesflankingtothePi-khlocuswasselectedfortheinvestigation.Atotalof16genesinindicaand15genesinjaponicawerepredictedandanno-tatedinthisregion.TheaverageGCcontentofindicaandjaponicagenesinthisregionwas53.15%and49.3%,respectively.Bothindicaandjaponicasequenceswerepolymorphicforsimplesequencerepeatshavingmono-,di-,tri-,tetra-,andpentanucleotides.SequenceanalysisofthespecificblastresistantPi-khalleleofTetepandthesusceptiblePi-khalleleofthejaponicaricelineNipponbareshoweddifferencesinthenumberanddistributionofmotifsinvolvedinphosphorylation,resultingintheresistancephenotypeinTetep.
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:报道了内蒙古白粉菌4个新记录种,分别是寄生在白桦Betulaplatyphylla上的桦木白粉菌Erysiphebetulina、大果榆Ulmusmacrocarpa上的榆白粉菌原变种Erysipheulmivar.ulmi、刺果茶藤Ribesburejense上的醋栗单囊白粉菌Podosphaeramors-uvae和栾树Koelreuteriapaniculata上的栾树叉钩丝壳Sawadaeakoelreuteriae。其中,白桦Betulaplatyphylla和刺果茶蔗子Ribesburejense为上述白粉菌的国内新记录寄主,文中提供了详细的形态描述和线条图。引证标本保存在赤峰学院菌物标本室(CFSZ)。
简介:Asimplemethodtocreateachromosome-specificDNAlibrqaryofrice,includingmicrodissection,amplification,charterizationandcloning,isdescribed.Ricechromosome4fromametaphasecellhasbeenisolatedandamplifiedbytheLinkerAdapterPCR(LA-PCR).ThePCRproductswerelabeledasprobeswithDIG-11-dUTPusingtherandomprimingmethod.SouthernblotanalysiswithricegenomicDNAandspecificRFLPmarkersdemonstratedthatthePCRproductswerederivedfromricechromosome4.Alargelibrarycomprisingover100,000recombinantplasmidmicroclonesfromricechromosome4wasconstructed.Colonyhybridizationshowedthat58%oftheclonescontainedsingleorlow-copysequencesand42%containedrepetitivesequences.ThesizeofinsertsgeneratedbyPCRrangedfrom140bpto500bp.ThismethodwillfacilitatecloningofthespecificchromosomeDNAmarkersandimportantgenesofrice.