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    當前位置 : Millipore >>> Millipore/05-348 | Anti-Tau Antibody, clone 5E2/05-348/200 µg
    Millipore/05-348 | Anti-Tau Antibody, clone 5E2/05-348/200 µg
    • Millipore/05-348 | Anti-Tau Antibody, clone 5E2/05-348/200 µg

    Millipore/05-348 | Anti-Tau Antibody, clone 5E2/05-348/200 µg

    價格: ¥5184.00 市場價: 8640.00

    貨號: 05-348
    品牌: Millipore
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      • Description
        CatalogueNumber05-348
        ReplacesMAB10417
        BrandFamilyUpstate
        TradeName
        • Upstate
        DescriptionAnti-TauAntibody,clone5E2
        ProductInformation
        FormatPurified
        Presentation0.1MTris-glycine,pH7.4,containingand0.05%sodiumazide
        StorageandShippingInformation
        StorageConditions2yearsat-20°C
        Applications
        ApplicationDetectTauusingthisAnti-TauAntibody,clone5E2validatedforuseinWB,IH.
        KeyApplications
        • WesternBlotting
        • Immunohistochemistry
        BIOLOGicalInformation
        ImmunogenFetalheatstableMAPS
        Cloneclone5E2
        HostMouse
        SpecificityseveralpartsofTauproteinbetween50kDaand70kDa
        IsotypeIgG1
        SpeciesReactivity
        • Bovine
        • Human
        • Mouse
        • Rat
        • Rabbit
        AntibodyTypeMonoclonalAntibody
        EntrezGeneNumber
        EntrezGeneSummaryThisgeneencodesthemicrotubule-associatedproteintau(MAPT)whosetranscriptundergoescomplex,regulatedalternativesplicing,givingrisetoseveralmRNAspecies.MAPTtranscriptsaredifferentiallyexpressedinthenervoussystem,dependingonstageofneuronalmaturationandneurontype.MAPTgenemutationshavebeenassociatedwithseveralneurodegenerativedisorderssuchasAlzheimer"sdisease,Pick"sdisease,frontotemporaldementia,cortico-basaldegenerationandprogressivesupranuclearpalsy.
        GeneSymbol
        • MAPT
        • MTBT2
        • tau
        • FTDP-17
        • MSTD
        • TAU
        • MTBT1
        • PHF-tau
        • MGC138549
        • MAPTL
        • FLJ31424
        • DDPAC
        • PPND
        PurificationMethodProteinGChromatography
        UniProtNumber
        UniProtSummaryFUNCTION:SwissProt:P10636#PromotesmicrotubuleassemblyandstABIlity,andmightbeinvolvedintheestablishmentandmaintenanceofneuronalpolarity.TheC-terminusbindsaxonalmicrotubuleswhiletheN-terminusbindsneuralplasmamembranecomponents,suggestingthattaufunctionsasalinkerproteinbetweenboth.Axonalpolarityispredeterminedbytaulocalization(intheneuronalcell)inthedomainofthecellbodydefinedbythecentrosome.TheshortisoformsallowplasticityoftheCytoskeletonwhereasthelongerisoformsmaypreferentiallyplayaroleinitsstabilization.
        SIZE:758aminoacids;78878Da
        SUBUNIT:InteractswithPSMC2throughSQSTM1(Bysimilarity).InteractswithSQSTM1whenpolyubiquitinated.
        SUBCELLULARLOCATION:Cytoplasm,cytosol.Cellmembrane.Note=Mostlyfoundintheaxonsofneurons,inthecytosolandinassociationwithplasmamembranecomponents.
        TISSUESPECIFICITY:Expressedinneurons.IsoformPNS-tauisexpressedintheperipheralnervoussystemwhiletheothersareexpressedinthecentralnervoussystem.DEVELOPMENTALSTAGE:Four-repeat(typeII)tauisexpressedinanadult-specificmannerandisnotfoundinfetalbrain,whereasthree-repeat(typeI)tauisfoundinbothadultandfetalbrain.
        DOMAIN:SwissProt:P10636Thetau/MAPrepeatbindstotubulin.TypeIisoformscontain3repeatswhiletypeIIisoformscontain4repeats.
        PTM:PhosphorylationatserineandthreonineresiduesinS-PorT-Pmotifsbyproline-directedproteinkinases(PDPK:CDC2,CDK5,GSK-3,MAPK)(only2-3sitesperproteinininterphase,seven-foldincreaseinmitosis,andinPHF-tau),andatserineresiduesinK-X-G-SmotifsbyMAP/microtubuleaffinity-regulatingkinase(MARK)inAlzheimerdiseasedbrains.Phosphorylationdecreaseswithage.Phosphorylationwithintau"srepeatdomainorinflankingregionsseemstoreducetau"sinteractionwith,respectively,microtubulesorplasmamembranecomponents.PhosphorylationonSer-610,Ser-622,Ser-641andSer-673inseveralisoformsduringmitosis.&Polyubiquitinated.RequiresfunctionalTRAF6andmayprovokeSQSTM1-dependentdegradationbytheproteasome(Bysimilarity).PHF-taucanbemodifiedbythreedifferentformsofpolyubiquitination."Lys-48"-linkedpolyubiquitinationisthemajorform,"Lys-6"-linkedand"Lys-11"-linkedpolyubiquitinationalsooccur.&GlycationofPHF-tau,butnotnormalbraintau.Glycationisanon-enzymaticpost-translationalmodificationthatinvolvesacovalentlinkagebetweenasugarandanaminogroupofaproteinmoleculeformingketoamine.Subsequentoxidation,fragmentationand/orcross-linkingofketoamineleadstotheproductionofadvancedglycationendproducts(AGES).GlycationmayplayaroleinstabilizingPHFaggregationleADIngtotangleformationinAD.
        DISEASE:SwissProt:P10636#InAlzheimerdisease,theneuronalcytoskeletoninthebrainisprogressivelydisruptedandreplacedbytanglesofpairedhelicalfilaments(PHF)andstraightfilaments,mainlycomposedofhyperphosphorylatedformsofTAU(PHF-TAUorADP-TAU).&DefectsinMAPTareacauseoffrontotemporaldementiaandparkinsonismlinkedtochromosome17(FTDP17)[MIM:600274,172700];alsocalledfrontotemporaldementia(FTD)orhistoricallytermedPickcomplex.Thisformoffrontotemporaldementiaischaracterizedbypreseniledementiawithbehavioralchanges,deteriorationofcognitivecapacitiesandlossofmemory.Insomecases,parkinsoniansymptomsareprominent.Neuropathologicalchangesincludefrontotemporalatrophyoftenassociatedwithatrophyofthebasalganglia,substantianigra,amygdala.Inmostcases,proteintaudepositsarefoundinglialcellsand/orneurons.&DefectsinMAPTareacauseofpallido-ponto-nigraldegeneration(PPND)[MIM:168610].Theclinicalfeaturesincludeocularmotilityabnormalities,dystoniaandurinaryincontinence,besidesprogressiveparkinsonismanddementia.&DefectsinMAPTareacauseofcorticobasaldegeneration(CBD).Itismarkedbyextrapyramidalsignsandapraxiaandcanbeassociatedwithmemoryloss.NeuropathologicfeaturesmayoverlapAlzheimerdisease,progressivesupranuclearpalsy,andParkinsondisease.&DefectsinMAPTareacauseofprogressivesupranuclearpalsy(PSP)[MIM:601104,260540];alsoknownasSteele-Richardson-Olszewskisyndrome.PSPischaracterizedbyakinetic-rigidsyndrome,supranucleargazepalsy,pyramidaltractdysfunction,pseudobulbarsignsandcognitivecapacitiesdeterioration.Neurofibrillarytanglesandgliosisbutnoamyloidplaquesarefoundindiseasedbrains.Mostcasesappeartobesporadic,withasignificantassociationwithacommonhaplotypeincludingtheMAPTgeneandtheflankingregions.Familialcasesshowanautosomaldominantpatternoftransmissionwithincompletepenetrance;geneticanalysisofafewcasesshowedtheoccurrenceoftaumutations,includingadeletionofAsn-613.&DefectsinMAPTmaybeacauseofhereditarydysphasicdisinhibitiondementia(HDDD)[MIM:607485].HDDDisafrontotemporaldementiacharacterizedbyprogressivecognitivedeficitswithmemorylossandpersonalitychanges,severedysphasicdisturbancesleadingtomutism,andhyperphagia.
        SIMILARITY:Contains4Tau/MAPrepeats.
        MolecularWeight50-70kDa
        PhysicochemicalInformation
        Dimensions
        MaterialsInformation
        MaterialsInformation
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