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PhosphoSolutions/CaM Kinase II (Thr286) Antibody/p1005-286/100 µl

价格
¥4574.70
货号:p1005-286
浏览量:127
品牌:PhosphoSolutions
服务
全国联保
正品保证
正规发票
签订合同
商品描述

Rabbitpolyclonalantibody

PooledSerum
Size:
100µl
Formulation:
AffinityPurifiedfromPooledSerum
Specificity:
Mouse,Rat,Human,Zenopus
Applications:
WB1:1000
Species:
Rabbit
GeneName:
CAMK2A/B
MolecularReference:
~50kDa
CiteThisAntibody:
PhosphoSolutionsCat#p1005-286,RRID:AB_2492051
Antigen/Purification:ExpandCollapse

Theantigenisaphosphopeptidecorrespondingtoaminoacidresiduessurroundingthephospho-Thr286foundinratbrainCaMKinaseII.

Theantibodyispreparedfrompooledrabbitserumbyaffinitypurificationviasequentialchromatographyonphospho-anddephospho-peptideaffinitycolumns.

 

BIOLOGicalSignificance:ExpandCollapse

Ca2+/calmodulin-dependentproteinkinaseII(CaMKinaseII)isamulti-functionalcalciumandcalmodulin-dependentproteinkinasethatmediatescellularresponsestoawidevarietyofintercellularsignals(Kennedy,1998;SchulmanandHanson,1993).CaMKinaseIIhasbeenshowntoregulatediversecellularfunctionsincludingsynapticplasticity,neurotransmittersynthesisandrelease,geneexpression,ionchannelfunction,carbohydratemetabolism,cytoskeletalfunction,andCa2+-homeostasis(Gleasonetal.,2003;Soderling,2000;HudmonandSchulman,2002).PhosphorylationofThr286onthekinaseproducesanautonomouslyactiveformofCaMKinaseII(Mengetal.,2003;Picciottoetal.,1993).AutophosphorylationofThr305inhibitstheactivityCaMKinaseII.PhosphorylationatthissiteappearstoreducetheassociationofCaMKinaseIIwiththePSDandreduceLTPandlearning(Elgersmaetal.,2002).

Storage

100µlin10mMHEPES(pH7.5),150mMNaCl,100µgBSApermland50%glycerol.Adequateamountofmaterialtoconduct10-miniWesternBlots.

Forlongtermstorage–20°Cisrecommended.Stableat–20°Cforatleast1year.

ProductSpecificReferences

Murakoshi,H.,Shin,M.E.,Parra-Bueno,P.,Szatmari,E.M.,Shibata,A.C.andYasuda,R.,2017.KineticsofEndogenousCaMKIIRequiredforSynapticPlasticityRevealedbyOptogeneticKinaseInhibitor.Neuron.Apr5;94(1):37-47.e5.PMID:28318784

Huang,L.,Hayes,S.andYang,G.,2016.Long-lastingbehavioraleffectsinneonatalmicewithmultipleexposuresto…-xylazineanesthesia.NeurotoxicologyandTeratology.PMID:27622724

Barcomb,K.,Buard,I.,Coultrap,S.J.,Kulbe,J.R.,O’Leary,H.,Benke,T.A.,&Bayer,K.U.(2014).AutonomousCaMKIIrequiresfurtherstimulationbyCa2+/calmodulinforenhancingsynapticstrength.TheFASEBJournal,28(8),3810-3819.PMID:24843070

Bernard,P.B.,Castano,A.M.,Bayer,K.U.,&Benke,T.A.(2014).Necessary,butnotsufficient:insightsintothemechanismsofmGluRmediatedlong-termdepressionfromaratmodelofearlylifeseizures.Neuropharmacology,84,1-12.PMID:24780380

StevenJ.Coultrap,K.UlrichBayer(2014)NitricoxideinducesCa2+-independentactivityoftheCa2+/calmodulin-dependentproteinkinaseII(CaMKII).J.BiolChem.289(28):19458-65.PMID:24855644

Magupalli,V.G.,Mochida,S.,Yan,J.,Jiang,X.,Westenbroek,R.E.,Nairn,A.C.,Scheuer,T.,&Catterall,W.A.(2013).Ca2+-independentactivationofCa2+/calmodulin-dependentproteinkinaseIIboundtotheC-terminaldomainofCaV2.1calciumchannels.JournalofBiologicalChemistry,288(7),4637-4648.PMID: 23255606

W.WadeKothmann,E.BradyTrexler,ChristopherM.Whitaker,WeiLi,StephenC.Massey,andJohnO’Brien(2012)NonsynapticNMDAReceptorsMediateActivity-DependentPlasticityofGapJunctionalCouplingintheAllAmacrineCellNetwork.J.Neurosci.32(3):6747-6759.PMID:22593045

RebekahS.Vest,HeatherO’Leary,StevenJ.Coultrap,MarkS.Kindy,andK.UlrichBayer(2010)EffectivePost-insultNeuroprotectionbyaNovelCa2+/Calmodulin-dependentProteinKinaseII(CaMKII)InhibitorJ.Biol.Chem.,285:20675–20682.PMID:20424167

StevenJ.Coultrap,IsabelleBuard,JaquelineR.Kulbe,MarkL.Dell’Acqua,andK.UlrichBayer(2010)CaMKIIAutonomyIsSubstrate-dependentandFurtherStimulatedbyCa2+/CalmodulinJ.Biol.Chem.,285:17930–17937.PMID:20353941

KurtisD.Davies,SusanM.Goebel-Goody,StevenJ.Coultrap,andMichaelD.Browning(2008)LongTermSynapticDepressionThatIsAssociatedwithGluR1DephosphorylationbutNotAmino-3-hydroxy-5-methyl-4-isoxazolepropionicAcid(AMPA)ReceptorInternalizationJ.Biol.Chem.,283:33138–33146.PMID:18819923

XiuSun,MichaelMilovanovic,YunZhao,andMarinaE.Wolf(2008)AcuteandChronicDopamineReceptorStimulationModulatesAMPAReceptorTraffickinginNucleusAccumbensNeuronsCoculturedwithPrefrontalCortexNeurons.J.Neurosci.,28:4216–4230.PMID:18417701

MatthewTownsend,TapanMehta,andDennisJ.Selkoe(2007)SolubleA-betaInhibitsSpecificSignalTransductionCascadesCommontotheInsulinReceptorPathway.J.Biol.Chem.,282:33305–33312.PMID:17855343

RebekahS.Vest,KurtisD.Davies,HeatherO’Leary,J.DavidPort,andK.UlrichBayer(2007)DualMechanismofaNaturalCaMKIIInhibitor.Mol.Biol.Cell,18:5024–5033.PMID:17942605

我们很高兴地宣布 PhosphoSolutions 的创始人兼首席执行官 Michael Browning 博士被任命为享有盛誉的 2020 年 CiteAb 终身成就奖的获得者。该奖项突出了一位在试剂领域产生重大影响的杰出人士。在长达四年的职业生涯中,布朗宁博士作为模范神经科学家、导师和商业领袖为科学发现事业服务。他无懈可击的诚信和对科学严谨性的奉献激励了无数研究生、博士后和员工,并在试剂行业树立了卓越标准。Browning 博士为研究界贡献可靠抗体的使命始于 1980 年代他在诺贝尔奖获得者 Paul Greengard 博士在耶鲁大学的实验室的博士后期间。在研究突触蛋白在突触功能中的关键作用时,他亲眼目睹了抗体质量与杰出研究成果之间的联系。作为科罗拉多大学药理学和神经科学系教授,Browning 博士开发了针对 LTP 所涉及蛋白质的抗体,LTP 被广泛认为是学习和记忆的关键细胞机制。1990 年代初期,美国国立卫生研究院 (NIH) 认可布朗宁博士对抗体作为研究工具的理解,并授予他开发其他新型抗体的资助。随后的许多出版物都引用了他的本土抗体,NIH 敦促他将他的工作商业化——从而开发了 PhosphoSolutions。由于多克隆抗体的多功能性和稳定性,布朗宁博士长期以来一直是多克隆抗体的支持者。在出现“重现性危机”之前,他是倡导试剂重现性的行业领导者。2006 年,在他的指导下,PhosphoSolutions 发起了一项行业内独一无二的血清汇集计划,只有在大量血清被积聚、阳性筛选然后汇集后才会释放抗体。这种做法保证了从同质起始材料中纯化的给定抗体的 20 年供应,几乎没有批次间的差异。认识到 Browning 博士在可重复性方面的领导地位,GBSI 邀请他参加其具有里程碑意义的 2016 年抗体验证研讨会,Browning 博士呼吁抗体制造商采用血清混合并改进和标准化内部验证。2019 年 9 月,Browning 博士加入了 PhosphoSolutions with Antibodies Incorporated 和 Aves Labs,组成了一个小型制造商家族,提供研究人员可以依赖的试剂。Browning 博士有一个妻子和两个成年儿子。在业余时间,他喜欢打高尔夫球并与家人共度时光。CiteAb 的创始人 Andrew Chalmers 博士说:“我个人祝贺 Michael Browning 博士获得 CiteAb 终身成就奖。任何见过他的人都会对他为研究界改进抗体的热情和奉献精神印象深刻。这是在成就非凡的职业生涯之后当之无愧的奖项。我和整个 CiteAb 团队向布朗宁博士表示祝贺