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简介：树枝状的房间(DC)在造血的房间的一张次要的人口，生产类型我干扰素(IFN)和另外的cytokines并且为天生的免疫是必要的。他们也是有势力抗原演讲者并且调整适应免疫。在DC子类型血浆之中似细胞的DC(pDC)生产类型的最高的数量我IFN。另外，象IL-12和IL-10那样的支持inflammatory和反煽动性的cytokines响应象发信号的受体(TLR)一样并且在病毒的感染之上的代价在DC被导致。在IRF家庭的蛋白质控制DC活动的许多方面。IRF-8和IRF-4为DC开发是必要的。他们差别控制四个DC子集的开发。IRF-8-/-老鼠大部分缺乏pDC和CD8alpha+DC，当IRF-4-/-老鼠缺乏CD4+DC时。IRF-8-/-，IRF4-/-，两倍猛烈老鼠有仅仅很少CD8a-CD4-DC那缺乏MHCII。IRF蛋白质也控制类型我在DC的IFN正式就职。IRF-7，在TLR发信号之上激活不仅在pDC，而且在常规DC(cDC)为IFN正式就职被要求，non-DC房间打字。IRF-3贡献在成纤维细胞感应的IFN，在在DC感应的IFN是非必需的。我们的最近的证据揭示那种类型我在DC感应的IFN非常依赖于IRF-8，它在DC在IFN基因正式就职的反馈阶段行动。类型我在pDC感应的IFN被MyD88调停依赖发信号小径，并且不同于在另外的房间采用的小径，它主要依靠TLR3和RIG-I家庭蛋白质。另外的支持inflammatorycytokines以一种IRF-5依赖方式被生产。然而，IRF-5没为IFN正式就职被要求，建议为类型的正式就职的分开的机制的存在我IFN和其它支持inflammatorycytokines。激活的DC接着生产的IFN和另外的cytokines预付DC成熟并且改变DC的显型和功能。这些过程也是可能的被IRF家庭蛋白质管理。

简介：CellsregulatephospholipaseD(PLD)activityinresponsetonumerousextracellularsignals.Here,weinvestigatedtheinvolvementofPLDactivityintransforminggrowthfactor-β(TGF-β1)-mediatedgrowthinhibitionofepithelialcells.TGF-β1)-mediatedgrowthinhibitionofepithelialcells.TGF-β1inhibitsthegrowthofMDCK,Mv1Lu,andA-549cells.Inthepresenceof0.4%butanol,TGF-β1inducesanincreaseintheformationofphosphatidylbutanol,auniqueproductcatalyzedbyPLD.TGF-β1alsoinducesanincreaseinphosphatidicacid(PA)levelinA-549andMDCKcells.TGF-β1inducesanincreaseinthelevelsofDAGlabeledwith[^3H]-myristicacidinA-549andMDCKcellsbutnotinMv1Lucells.NoincreaseofDAGwasobservedincellsprelabeledwith[^3H]-arachidonicacid.ThedatapresentedsuggestthatPLDactivationisinvolvedintheTGF-β1-inducedcellgrowthinhibition.

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简介：现在的学习试图定义postsynaptic的角色在多巴胺(DA)的规定的密度(PSD)-95受体功能。我们发现PSD-95身体上在co-transfectedHEK-293房间与D1或D2DA受体联系。DA受体的刺激以一种时间依赖者方式改变了在D1受体和PSD-95之间的协会。功能的试金显示PSD-95合作表示没影响D1刺激受体的营地生产，Gs蛋白质激活或受体不敏感性。然而，PSD-95由支持受体再循环加速了使内在化的膜受体的恢复，因此导致使内在化的D1受体的提高的促进感受性。我们的结果提供新奇机制因为调整再循环那的DA受体可以在postsynapticDA功能的调整和synapticneuroplasticity起一个重要作用。

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.