简介：Wedevelopedatransientmodelforactin-basedmotility.Diffusionofactinmonomerswasincludedintheformulationanditsinfluenceonthespeedofactin-drivencargoswasexaminedindetail.Ourresultsclearlydemonstratedhowactinpolymerizationacceleratescargosthatareinitiallystationary,aswellashowsteady-stateiseventuallyreached.Wealsofoundthat,duetopolymerizationanddiffusion,actinmonomerconcentrationneartheloadsurfacecanbesignificantlylowerthanthatintherestofth...

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简介：Inflammasomes是由响应病原体暴露或细胞的损坏便于煽动性的cytokines的版本调整天生的有免疫力的反应的多蛋白质建筑群。支持inflammatoryinflammasome发信号是重要的招待防卫，帮助开始跟随侮辱到主机，而是罐头的织物修理的进程有害，当过多或长期时。因此，inflammasome活动紧被调整。这里，我们讨论inflammasome规定的一批评机制，ubiquitination，那作为蛋白质稳定性和trafficking的一个通用调节的人工作。最近的研究由蛋白质ubiquitination提供了重要卓见进inflammasome激活的规定。明确地，当它联系到ubiquitination，我们考察inflammasome功能的分子的规定，并且讨论含意让治疗学的发展明确地指向异常inflammasome发信号。

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简介：幼芽的中心kinases(GCK)参予需要包括apoptosis，房间增长，极性和移植调整细胞的函数的许多发信号的小径。最近的研究证明了GCK是在适应、天生的有免疫力的规定的参加者。然而，微分激活和GCK的规章的机制，以及在上游、下游的发信号的分子，尚待充分被定义。它仍然保持未解决是否并且怎么GCK可以有存在的串音表明小径。这评论在与免疫系统相关的GCK的研究强调进步。

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简介：MicroRNAs(miRNAs)areaclassofshort,endogenously-initiatednon-codingRNAsthatpost-transcriptionallycontrolgeneexpressionviaeithertranslationalrepressionormRNAdegradation.ItisbecomingevidentthatmiRNAsareplayingsignificantrolesinregulatorymechanismsoperatinginvariousorganisms,includingdevelopmentaltimingandhost-pathogeninteractionsaswellascelldifferentiation,proliferation,apoptosisandtumorigenesis.Likewise,asaregulatoryelement,miRNAitselfiscoordinativelymodulatedbymultifariouseffectorswhencarryingoutbasicfunctions,suchasSNP,miRNAediting,methylationandcircadianclock.Thismini-reviewsummarizedthecurrentunderstandingofinteractionsbetweenmiRNAsandtheirtargets,includingrecentadvancementsindecipheringtheregulatorymechanismsthatcontrolthebiogenesisandfunctionalityofmiRNAsinvariouscellularprocesses.

简介：MicroRNAs(miRNAs)aresmall,non-codingsingle-strandedRNAsthatcanmodulatetargetgeneexpressionatposttranscriptionallevelandparticipateincellproliferation,differentiation,andapoptosis.Tcellshaveimportantfunctionsinacquiredimmuneresponse;miRNAsregulatethisimmuneresponsebytargetingthemRNAsofgenesinvolvedinTcelldevelopment,proliferation,differentiation,andfunction.Forinstance,miR-181familymembersfunctioninprogressionbytargetingBcl2andCD69,amongothers.MiR-17tomiR-92clustersfunctionbybindingtoCREB1,PTEN,andBim.ConsideringthatthesuppressionofTcell-mediatedimmuneresponsesagainsttumorcellsisinvolvedincancerprogression,weshouldinvestigatethemechanismbywhichmiRNAregulatesTcellstodevelopnewapproachesforcancertreatment.

简介：Regulationrelatesto.FoodpackagingadoitivesMedicalpackagingadditives.FlameRetaradantPlasticizer.Plasticizer.Antimicrobial.Colorant.

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简介：AIMToinvestigatetheeffectofgingeroloncolonicmotilityandtheactionofL-typecalciumchannelcurrentsinthisprocess.METHODS：ThedistalcolonwascutalongthemesentericborderandcleanedwithCa^2＋-freephysiologicalsalinesolution.MusclestripswereremovedandplacedinCa^2＋-freephysiologicalsalinesolution,whichwasoxygenatedcontinuously.Longitudinalsmoothmusclesampleswerepreparedbycuttingalongthemusclestripsandwerethenplacedinachamber.Mechanicalcontractileactivitiesofisolatedcolonicsegmentsinratswererecordedbya4-channelphysiograph.Colonsmoothmusclecellsweredissociatedbyenzymaticdigestion.L-typecalciumcurrentswererecordedusingtheconventionalwhole-cellpatch-clamptechnique.RESULTS：Gingerolinhibitedthespontaneouscontractionofcoloniclongitudinalsmoothmuscleinadose-dependentmannerwithinhibitionpercentagesof13.3%±4.1%,43.4%±3.9%,78.2%±3.6%and80.5%±4.5%at25μmol/L,50μmol/L,75μmol/Land100μmol/L,respectively（P〈0.01）.Nifedipine,anL-typecalciumchannelblocker,diminishedtheinhibitionofcolonicmotilitybygingerol.GingerolinhibitedL-typecalciumchannelcurrentsincoloniclongitudinalmyocytesofrats.Ata75μmol/Lconcentrationofgingerol,thepercentageofgingerolinducedinhibitionwasdiminishedbynifedipinefrom77.1%±4.2%to42.6%±3.6%（P〈0.01）.GingerolsuppressedIBainadose-dependentmanner,andtheinhibitionrateswere22.7%±2.38%,35.77%±3.14%,49.78%±3.48%and53.78%±4.16%ofcontrolat0mV,respectively,atconcentrationsof25μmol/L,50μmol/L,75μmol/Land100μmol/L（P〈0.01）.Thesteady-stateactivationcurvewasshiftedtotherightbytreatmentwithgingerol.Thevalueofhalfactivationwas-14.23±1.12mVinthecontrolgroupand-10.56±1.04mVinthe75μmol/Lgroup（P〈0.05）withslopefactors,Ks,of7.16±0.84and7.02±0.93（P〈0.05）inthecontroland75μmol/Lgroups,respectively.However,thesteady-st