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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(jià)格: ￥4560.00 市場價(jià): 7600.00
貨號(hào): 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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