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℡ 4000-520-616
℡ 4000-520-616
Millipore/AB9668 | Anti-Tau phospho Threonine 231 Antibody/AB9668/100 µL
产品编号:AB9668
市  场 价:¥7800.00
场      地:美国(厂家直采)
产品分类: 抗体类>一抗>功能性抗体>
联系QQ:1570468124
电话号码:4000-520-616
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美  元  价:$390.00
品      牌: Millipore
公      司:Millipore
公司分类:
Millipore/AB9668 | Anti-Tau phospho Threonine 231 Antibody/AB9668/100 µL
商品介绍
Description
CatalogueNumberAB9668
BrandFamilyChemicon®
TradeName
  • Chemicon
DescriptionAnti-TauphosphoThreonine231Antibody
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.Threonine231isphosphorylatedbyGSK-3beta,cdk5andcdk1andhasbeenshowntobeinvolvedinthepre-tangleprocessofAD.
ProductInformation
FormatAffinityPurified
PresentationAffinitypurifiedimmunoglobulin.LiquidinDulbecco"sPBS(withoutMg2+andCa2+),pH7.3,50%glycerolwith1.0mg/mLBSAand0.05%sodiumazide.
StorageandShippingInformation
StorageConditionsMaintainat-20°Cinundilutedforupto6monthsafterdateofreceipt.Avoidrepeatedfreeze/thawcycles.Donotstoreinaselfdefrostingfreezer.
Applications
ApplicationAnti-TauphosphoThreonine231AntibodydetectslevelofTauphosphoThreonine231&hasbeenpublished&validatedforuseinWB.
KeyApplications
  • WesternBlotting
ApplicationNotesWesternblot:1:1,000.Suggestedblockingbufferis5%BSA-TBSTforonehouratroomtemperature.Suggestedantibodydilutionbufferis1%BSA-TBST.Suggestedantibodyincubationtimeis2hoursatroomtemperature..

Optimalworkingdilutionsmustbedeterminedbytheenduser.
BIOLOGicalInformation
ImmunogenSyntheticpeptideofaminoacidssurroundingthephosphoThreonine231siteofhumanTau.
HostRabbit
SpecificityTauphosphoThreonine231.TheantibodyrecognizesTaupThreonine231insamplesofrecombinanthumanTautreatedwithGSK-3betafor45minutes.ThereactivityoftheantibodyisblockedwiththepThreonine231peptidebutnotthenon-phosphopeptideoragenericphosphoThreonine-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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