当前位置 ： Millipore >>> Millipore/AB9672 | Anti-Tau phospho Serine 214 Antibody/AB9672/100 µL
Millipore/AB9672 | Anti-Tau phospho Serine 214 Antibody/AB9672/100 µL
  • Millipore/AB9672 | Anti-Tau phospho Serine 214 Antibody/AB9672/100 µL

Millipore/AB9672 | Anti-Tau phospho Serine 214 Antibody/AB9672/100 µL

价格: ¥4680.00 市场价: 7800.00
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货号: AB9672
品牌: Millipore
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    • Description
      CatalogueNumberAB9672
      BrandFamilyChemicon®
      TradeName
      • Chemicon
      DescriptionAnti-TauphosphoSerine214Antibody
      BackgroundInformationTauisaneuronalmicrotubule-associatedproteinfoundpredominantlyonaxonsandfunctionstopromotetubulinpolymerizationandstABIlizemicrotubules.Tau,initshyperphosphorylatedform,isthemajorcomponentofpairedhelicalfilaments(PHF),thebuildingblockofneurofibrillarylesionsinAlzheimer"sdisease(AD)brain.HyperphosphorylatedTauisalsofoundinneurofibrillarylesionsinarangeofothercentralnervoussystemdisorders.HyperphosphorylationimpairsthemicrotubulebindingfunctionofTau,resultinginthedestabilizationofmicrotubulesinADbrains,ultimatelyleADIngtothedegenerationoftheaffectedneurons.Numerousserine/threoninekinases,includingGSK-3beta,proteinkinaseA(PKA),cyclin-dependentkinase5(cdk5)andcaseinkinaseII(CK2),phosphorylateTau.Serine214isphosphorylatedbyGSK-3betainADbrain.
      ProductInformation
      FormatAffinityPurified
      PresentationAffinitypurifiedimmunoglobulin.LiquidinDulbecco"sPBS(withoutMg2+andCa2+),pH7.3,50%glycerolwith1.0mg/mLBSAand0.05%sodiumazide.
      StorageandShippingInformation
      StorageConditionsMaintainat-20°Cinundilutedforupto6monthsafterdateofreceipt.Avoidrepeatedfreeze/thawcycles.Donotstoreinaselfdefrostingfreezer.
      Applications
      ApplicationThisAnti-TauphosphoSerine214AntibodyisvalidatedforuseinWBforthedetectionofTauphosphoSerine214.
      KeyApplications
      • WesternBlotting
      ApplicationNotesWesternblot:1:1,000.Suggestedblockingbufferis5%BSA-TBSTforonehouratroomtemperature.Suggestedantibodydilutionbufferis1%BSA-TBST.Suggestedantibodyincubationtimeis2hoursatroomtemperature.

      Optimalworkingdilutionsmustbedeterminedbytheenduser.
      BIOLOGicalInformation
      ImmunogenSyntheticpeptideofaminoacidssurroundingthephosphoSerine214siteofhumanTau.
      HostRabbit
      SpecificityTauphosphoSerine214.TheantibodyrecognizesTaupSerine214insamplesofrecombinanthumanTautreatedwithGSK-3betafor45minutes.ThereactivityoftheantibodyisblockedwiththepSerine214peptidebutnotthenon-phosphopeptideoragenericphosphoSerine-containingpeptide.
      SpeciesReactivity
      • Human
      AntibodyTypePolyclonalAntibody
      EntrezGeneNumber
      EntrezGeneSummaryThisgeneencodesthemicrotubule-associatedproteintau(MAPT)whosetranscriptundergoescomplex,regulatedalternativesplicing,givingrisetoseveralmRNAspecies.MAPTtranscriptsaredifferentiallyexpressedinthenervoussystem,dependingonstageofneuronalmaturationandneurontype.MAPTgenemutationshavebeenassociatedwithseveralneurodegenerativedisorderssuchasAlzheimer"sdisease,Pick"sdisease,frontotemporaldementia,cortico-basaldegenerationandprogressivesupranuclearpalsy.
      GeneSymbol
      • MAPT
      • MTBT2
      • MAPTL
      • PHF-tau
      • tau
      • DDPAC
      • FTDP-17
      • MGC138549
      • MSTD
      • TAU
      • FLJ31424
      • MTBT1
      • PPND
      Modifications
      • Phosphorylation
      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.
      PhysicochemicalInformation
      Dimensions
      MaterialsInformation
      MaterialsInformation
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