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    當前位置 ： Millipore >>> Millipore/AB5112 | Anti-Parkin Antibody, a.a. 305-323/AB5112/50 µL
    Millipore/AB5112 | Anti-Parkin Antibody, a.a. 305-323/AB5112/50 µL
    • Millipore/AB5112 | Anti-Parkin Antibody, a.a. 305-323/AB5112/50 µL

    Millipore/AB5112 | Anti-Parkin Antibody, a.a. 305-323/AB5112/50 µL

    價格: ￥4560.00 市場價: 7600.00
    打印產品信息
    貨號: AB5112
    品牌: Millipore
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      • Description
        CatalogueNumberAB5112
        BrandFamilyChemicon®
        TradeName
        • Chemicon
        DescriptionAnti-ParkinAntibody,a.a.305-323
        ProductInformation
        FormatSerum
        PresentationRabbitserum.Lyophilized.Reconstitutewith50μLofsteriledistilledwater.Centrifugetoremoveinsolublematerial.Containsnopreservative.
        StorageandShippingInformation
        StorageConditionsMaintainlyophilizedmaterialatat-20°Cto-70°Cforupto12monthsafterdateofreceipt.Afterreconstitutionmaintainat-20°Cto-70°Cinundilutedaliquotsforupto6months.Avoidrepeatedfreeze/thawcycles.Glycerol(ACSgradeorbetter)canbeadded(1:1)forgreaterstABIlity.
        Applications
        ApplicationDetectParkinusingthisAnti-ParkinAntibody,a.a.305-323validatedforuseinELISA,WB,IH.
        KeyApplications
        • ELISA
        • WesternBlotting
        • Immunohistochemistry
        ApplicationNotesImmunohistochemistry:1:1000-1:2000

        OnesiteELISA

        Westernblot:1:1000-1:2000(recognizesadoubletat44-52kDaonblotsofhumanbrain)

        Theimmunogenpeptideisavailable(cat#AG237)forpre-absorbtioncontrols.

        Optimalworkingdilutionsmustbedeterminedbytheenduser.
        BIOLOGicalInformation
        ImmunogenA19aminoacidpeptide(RILGEEQYNRYQQYGAEEC)correspondingtoaminoacids305-323ofthehumanparkinmolecule.Aninternalpeptidesequencewaschosentoavoidthepossibilityofcrossreactivitywithubiquitin.
        Epitopea.a.305-323
        HostRabbit
        SpecificityParkin.Parkinson"sdiseaseisacommonneurodegenerativediseaseiscausedbyslowdeathofneuronsinthesubstantialnigra,abrainregionthatutilizestheneurotransmitterdopamine.Parkin,arecentlydiscoveredgeneencodingalargeprotein,maybeinvolvedinnormalandabnormalproteindegradationincells.RecentevidenceindicatesthatpointmutationsintheParkingeneappeartoberesponsIBLeforthepathogenesisofsomeformsofParkinson"sdisease.
        SpeciesReactivity
        • Human
        • Rat
        AntibodyTypePolyclonalAntibody
        EntrezGeneNumber
        EntrezGeneSummaryTheprecisefunctionofthisgeneisunknown;however,theencodedproteinisacomponentofamultiproteinE3ubiquitinligasecomplexthatmediatesthetargetingofsubstrateproteinsforproteasomaldegradation.MutationsinthisgeneareknowntocauseParkinsondiseaseandautosomalrecessivejuvenileParkinsondisease.Alternativesplicingofthisgeneproducesmultipletranscriptvariantsencodingdistinctisoforms.Additionalsplicevariantsofthisgenehavebeendescribedbutcurrentlylacktranscriptsupport.
        GeneSymbol
        • PARK2
        • PDJ
        • PRKN
        • LPRS2
        • AR-JP
        • parkin
        • EC6.3.2.-
        UniProtNumber
        UniProtSummaryFUNCTION:SwissProt:O60260#FunctionswithinamultiproteinE3ubiquitinligasecomplex,catalyzingthecovalentattachmentofubiquitinmoietiesontosubstrateproteins.ThesesubstratesincludeSYT11,CCNE1,GPR37,STUB1,a22kDaO-linkedglycosylatedisoformofSNCAIPandSEPT5.Mayplayamoregeneralroleintheubiquitinproteasomalpathwaybyparticipatingintheremovaland/ordetoxificationofabnormallyfoldedordamagedprotein.LossofthisubiquitinligaseactivityappearstobethemechanismunderlyingpathogenesisofPARK2.Mayprotectneuronsagainstalphasynucleintoxicity,proteasomaldysfunction,GPR37accumulation,andkainate-inducedexcitotoxicity.Mayplayaroleincontrollingneurotransmittertraffickingatthepresynapticterminalandincalcium-dependentexocytosis.RegulatescyclinEduringneuronalapoptosis.Mayrepresentatumorsuppressorgene.
        SIZE:465aminoacids;51641Da
        SUBUNIT:FormsanE3ubiquitinligasecomplexwithUBE2L3orUBE2L6.PartofaSCF-likecomplex,consistingofPARK2,CUL1andFBXW7.InteractswithSNCAIP.BindstotheC2AandC2BdomainsofSYT11.InteractsandregulatestheturnoverofSEPT5.Partofacomplex,includingSTUB1,HSP70andGPR37.TheamountofSTUB1inthecomplexincreasesduringERstress.STUB1promotesthedissociationofHSP70fromPARK2andGPR37,thusfacilitatingPARK2-mediatedGPR37ubiquitination.HSP70transientlyassociateswithunfoldedGPR37andinhibitstheE3activityofPARK2,whereas,STUB1enhancestheE3activityofPARK2throughpromotionofdissociationofHSP70fromPARK2-GPR37complexes.InteractswithPSMD4andPACRG.InteractswithLRRK2.InteractswithRANBP2.InteractswithSUMO1butnotSUMO2,whichpromotesnuclearlocalizationandautoubiquitination.
        SUBCELLULARLOCATION:Cytoplasm.Note=Co-localizeswithSTY11inneutrites.Co-localizeswithSNCAIPinbrainstemLewybodies.Nucleus.
        TISSUESPECIFICITY:Highlyexpressedinthebrainincludingthesubstantianigra.Expressedinheart,testisandskeletalmuscle.Expressionisdown-regulatedorabsentintumorbiopsies,andabsentinthebrainofPARK2patients.Overexpressionprotectsdopamineneuronsfromkainate-mediatedapoptosis.
        DOMAIN:SwissProt:O60260Theubiquitin-likedomainbindsthePSMD4subunitof26Sproteasomes.
        PTM:Auto-ubiquitinatesinanE2-dependentmannerleADIngtoitsowndegradation.&S-nitrosylated.TheinhibitionofPARK2ubiquitinE3ligaseactivitybyS-nitrosylationcouldcontributetothedegenerativeprocessinPDbyimpairingtheubiquitinationofPARK2substrates.
        DISEASE:SwissProt:O60260#DefectsinPARK2areacauseofParkinsondisease(PD)[MIM:168600].PDisacomplex,multifactorialdisorderthattypicallymanifestsaftertheageof50years,althoughearly-onsetcases(before50years)areknown.PDgenerallyarisesasasporadicconditionbutisoccasionallyinheritedasasimplemendeliantrait.AlthoughsporadicandfamilialPDareverysimilar,inheritedformsofthediseaseusuallybeginatearlieragesandareassociatedwithatypicalclinicalfeatures.PDischaracterizedbybradykinesia,restingtremor,muscularrigidityandposturalinstability,aswellasbyaclinicallysignificantresponsetotreatmentwithlevodopa.ThepathologyofPDinvolvesthelossofdopaminergicneuronsinthesubstantianigraandthepresenceofLewybodies(intraneuronalaccumulationsofaggregatedproteins),insurvivingneuronsinvariousareasofthebrain.&DefectsinPARK2arethecauseofautosomalrecessiveearlyonsetParkinsondisease2(PARK2)[MIM:600116];alsoknownasearly-onsetparkinsonismwithdiurnalfluctuation(EPDF)orautosomalrecessivejuvenileParkinsondisease(PDJ).PARK2issymptomaticallydifferentinseveralaspectsfromidiopathicParkinsondisease,althoughclassicsymptomssuchasbradykinesia,rigidityandtremorarepresent.AdditionalclinicalfeaturesincludeearlyDOPA-induceddyskinesia,diurnalfluctuationofthesymptoms,sleepbenefit,dystoniaandhyper-reflexia.PARK2isusuallycharacterizedbyonsetbefore40,withameanageatonsetof23.2years.Pathologically,PARK2patientsshowlossofdopaminergicneuronsinthesubstantianigra,similartothatseeninParkinsondisease;however,Lewybodies(intraneuronalaccumulationsofaggregatedproteins)areabsent.&DefectsinPARK2maybeinvolvedinthedevelopmentand/orprogressionofovariancancer.
        SIMILARITY:Contains2IBR-typezincfingers.&Contains2RING-typezincfingers.&Contains1ubiquitin-likedomain.
        MISCELLANEOUS:Theparkinlocus(PRKN),adjacenttothe6qtelomereishyper-recombinableandlieswithinFRA6E,thethirdmostcommonfragilesiteintumortissue.
        PhysicochemicalInformation
        Dimensions
        MaterialsInformation
        MaterialsInformation
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