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Millipore/AB5334P | Anti-Synuclein α Antibody/AB5334P/50 µg
  • Millipore/AB5334P | Anti-Synuclein α Antibody/AB5334P/50 µg

Millipore/AB5334P | Anti-Synuclein α Antibody/AB5334P/50 µg

價格: ￥4680.00 市場價: 7800.00
貨號: AB5334P
品牌: Millipore
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    • Description
      CatalogueNumberAB5334P
      Replaces04-1053
      BrandFamilyChemicon®
      TradeName
      • Chemicon
      DescriptionAnti-SynucleinαAntibody
      ProductInformation
      FormatAffinityPurified
      PresentationAffinitypurifiedimmunoglobulin.Lyophilized.Reconstitutewith50μLofsteriledistilledwater.Centrifugetoremoveanyresidue.Glycerol(1:1)canbeaddedforadditionalstABIlity.
      StorageandShippingInformation
      StorageConditionsMaintainlyophilizedmaterialat-70°C(dry)forupto12months.Afterreconstitutionmaintainat-20°Cinundilutedaliquotsforupto6months.Avoidrepeatedfreeze/thawcycles.
      Applications
      ApplicationDetectSynucleinusingthisAnti-SynucleinAntibody,αvalidatedforuseinWB,IH(P).
      KeyApplications
      • WesternBlotting
      • Immunohistochemistry(Paraffin)
      ApplicationNotesImmunohistochemistry:0.5-1μg/mLonfrozenorparaffinsections.

      Westernblot:0.5-1μg/mL

      Optimalworkingdilutionsmustbedeterminedbytheenduser.
      BIOLOGicalInformation
      ImmunogenSyntheticpeptidecorrespondingaminoacids116-131ofhumanalphasynuclein.
      HostSheep
      SpecificityRecognizesalphasynuclein.
      SpeciesReactivity
      • Human
      • Rat
      AntibodyTypePolyclonalAntibody
      EntrezGeneNumber
      EntrezGeneSummaryAlpha-synucleinisamemberofthesynucleinfamily,whichalsoincludesbeta-andgamma-synuclein.Synucleinsareabundantlyexpressedinthebrainandalpha-andbeta-synucleininhibitphospholipaseD2selectively.SNCAmayservetointegratepresynapticsignalingandmembranetrafficking.DefectsinSNCAhavebeenimplicatedinthepathogenesisofParkinsondisease.SNCApeptidesareamajorcomponentofamyloidplaquesinthebrainsofpatientswithAlzheimer"sdisease.TwoalternativelysplicedtranscriptsofSNCAhavebeenidentified.Additionalsplicingmaybepresentbutthefull-lengthnatureofthesevariantshasnotbeendetermined.
      GeneSymbol
      • SNCA
      • PD1
      • alpha-synuclein
      • NACP
      • PARK4
      • MGC110988
      • PARK1
      • Alpha-synuclein
      UniProtNumber
      UniProtSummaryFUNCTION:SwissProt:P37840#Maybeinvolvedintheregulationofdopaminereleaseandtransport.Solubleprotein,normallylocalizedprimarilyatthepresynapticregionofaxons,whichcanformfilamentousaggregatesthatarethemajornonamyloidcomponentofintracellularinclusionsinseveralneurodegenerativediseases(synucleinopathies).Inducesfibrillizationofmicrotubule-associatedproteintau.Reducesneuronalresponsivenesstovariousapoptoticstimuli,leADIngtoadecreasedcaspase3activation.
      SIZE:140aminoacids;14460Da
      SUBUNIT:Solublemonomerwhichcanformfilamentousaggregates.InteractswithUCHL1(Bysimilarity).InteractswithphospholipaseDandhistones.
      SUBCELLULARLOCATION:Cytoplasm.Membrane.Nucleus.Note=Membrane-boundindopaminergicneurons.Alsofoundinthenucleus.
      TISSUESPECIFICITY:Expressedprincipallyinbrainbutisalsoexpressedinlowconcentrationsinalltissuesexaminedexceptinliver.Concentratedinpresynapticnerveterminals.
      DOMAIN:SwissProt:P37840TheNACdomainisinvolvedinthefibrilformation.Themiddleregionformsthecoreofthefilaments.TheC-terminusmayregulateaggregationanddeterminethediameterofthefilaments.
      PTM:Phosphorylated,predominantlyonserineresidues.PhosphorylationbyCK1appearstooccuronresiduesdistinctfromtheresiduephosphorylatedbyotherkinases.PhosphorylationofSer-129isselectiveandextensiveinsynucleinopathylesions.Invitro,phosphorylationatSer-129promotedinsolublefibrilformation.PhosphorylatedonTyr-125byaPTK2B-dependentpathwayuponosmoticstress.&Hallmarklesionsofneurodegenerativesynucleinopathiescontainalpha-synucleinthatismodifiedbynitrationoftyrosineresiduesandpossIBLybydityrosinecross-linkingtogeneratedstableoligomers.&Ubiquitinated.Thepredominantconjugateisthediubiquitinatedform(Bysimilarity).
      DISEASE:SwissProt:P37840#DefectsinSNCAareacauseofautosomaldominantParkinsondisease1(PARK1)[MIM:168601,168600].Parkinsondisease(PD)isacomplex,multifactorialdisorderthattypicallymanifestsaftertheageof50years,althoughearly-onsetcases(before50years)areknown.PDgenerallyarisesasasporadicconditionbutisoccasionallyinheritedasasimplemendeliantrait.AlthoughsporadicandfamilialPDareverysimilar,inheritedformsofthediseaseusuallybeginatearlieragesandareassociatedwithatypicalclinicalfeatures.PDischaracterizedbybradykinesia,restingtremor,muscularrigidityandposturalinstability,aswellasbyaclinicallysignificantresponsetotreatmentwithlevodopa.ThepathologyinvolvesthelossofdopaminergicneuronsinthesubstantianigraandthepresenceofLewybodies(intraneuronalaccumulationsofaggregatedproteins),insurvivingneuronsinvariousareasofthebrain.&DefectsinSNCAarethecauseofParkinsondisease4(PARK4)[MIM:605543,168600].&DefectsinSNCAarethecauseofLewybodydementia(DLB)[MIM:127750].DLBisaneurodegenerativedisorderclinicallycharacterizedbydementiaandparkinsonism,oftenwithfluctuatingcognitivefunction,visualhallucinations,falls,syncopalepisodes,andsensitivitytoneurolepticmedication.PresenceofLewybodiesaretheonlyessentialpathologicfeatures.&DepositionoffibrillaramyloidproteinsintraneuronallyasneurofibrillarytanglesischaracteristicofAlzheimerdisease(AD).SNCAisaminorproteinfoundwithinthesedeposits,butamajornonamyloidcomponent.&Brainironaccumulationtype1(NBIA1,alsocalledHallervorden-Spatzsyndrome),arareneuroaxonaldystrophy,ishistologicallycharacterizedbyaxonalspheroids,irondeposition,Lewybody(LB)-likeintraneuronalinclusions,glialinclusionsandneurofibrillarytangles.SNCAisfoundinLB-likeinclusions,glialinclusionsandspheroids.
      SIMILARITY:Belongstothesynucleinfamily.
      PhysicochemicalInformation
      Dimensions
      MaterialsInformation
      MaterialsInformation
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