當前位置 ： Millipore >>> Millipore/MAB5228 | Anti-Amyloid Precursor Protein Antibody, Secretory, clone OM84/MAB5228/100 µg
Millipore/MAB5228 | Anti-Amyloid Precursor Protein Antibody, Secretory, clone OM84/MAB5228/100 µg
  • Millipore/MAB5228 | Anti-Amyloid Precursor Protein Antibody, Secretory, clone OM84/MAB5228/100 µg

Millipore/MAB5228 | Anti-Amyloid Precursor Protein Antibody, Secretory, clone OM84/MAB5228/100 µg

價格: ￥4188.00 市場價: 6980.00
貨號: MAB5228
品牌: Millipore
規(guī)格
數(shù)量
庫存(0)
特別 提示
代購產(chǎn)品：無質(zhì)量問題不接受退換貨，下單前請仔細核對信息。
下單后請及時聯(lián)系客服核對商品價格，訂單生效后再付款。
資深產(chǎn)品顧問
咨詢顧問

全國免費服務熱線

4000-520-616

  • 自營商城 一站式服務
  • 廠家直采 剔除溢價
  • 品質(zhì)甄選 正品保證
  • 嚴控流程 只做188精品
  • 極速物流 如約送貨
  • 詳情
  • 使用說明
  • 常見問題
    • Description
      CatalogueNumberMAB5228
      BrandFamilyChemicon®
      TradeName
      • Chemicon
      DescriptionAnti-AmyloidPrecursorProteinAntibody,Secretory,cloneOM84
      AlternateNames
      • APP
      ProductInformation
      FormatPurified
      Control
      • Brain
      PresentationProteinAPurifiedmouseimmunoglobulinin10mMsodiumphosphatebuffer(pH7.4),0.15MNaCl,and0.1%sodiumazideasapreservative..
      StorageandShippingInformation
      StorageConditionsMaintainfrozenat-70°Corbelowinundilutedaliquotsforupto12months,avoidrepeatedfreeze/thawcycles.
      Applications
      ApplicationAnti-AmyloidPrecursorProteinAntibody,Secretory,cloneOM84detectslevelofAmyloidPrecursorProtein&hasbeenpublished&validatedforuseinELISA&WB.
      KeyApplications
      • ELISA
      • WesternBlotting
      ApplicationNotesWesternblot:10μg/mLELISA:1μg/mL

      Optimalworkingdilutionsmustbedeterminedbyenduser.
      BIOLOGicalInformation
      ImmunogenAmyloidPrecursorProtein(APP)secretedbytheEJ-1bladdercarcinomacellline.
      EpitopeSecretory
      CloneOM84
      ConcentrationPleaserefertotheCertificateofAnalysisforthelot-specificconcentration.
      HostMouse
      SpecificityReactswithsecretoryamyloidprecursorprotein(sAPP),butnotwithAmyloid-Betaprotein1-40.
      IsotypeIgG2aκ
      SpeciesReactivity
      • Human
      AntibodyTypeMonoclonalAntibody
      EntrezGeneNumber
      EntrezGeneSummaryThisgeneencodesacellsurfacereceptorandtransmembraneprecursorproteinthatiscleavedbysecretasestoformanumberofpeptides.SomeofthesepeptidesaresecretedandcanbindtotheacetyltransferasecomplexAPBB1/TIP60topromotetranscriptionalactivation,whileothersformtheproteinbasisoftheamyloidplaquesfoundinthebrainsofpatientswithAlzheimerdisease.MutationsinthisgenehavebeenimplicatedinautosomaldominantAlzheimerdiseaseandcerebroarterialamyloidosis(cerebralamyloidangiopathy).Multipletranscriptvariantsencodingseveraldifferentisoformshavebeenfoundforthisgene.
      GeneSymbol
      • APP
      • ABPP
      • PN-II
      • AD1
      • A4
      • CVAP
      • PN2
      • ABETA
      • CTFgamma
      • APPI
      • PreA4
      • AAA
      PurificationMethodProteinAPurfied
      UniProtNumber
      UniProtSummaryFUNCTION:SwissProt:P05067#Thegamma-CTFpeptidesaswellasthecaspase-cleavedpeptides,includingC31,arepotentenhancersofneuronalapoptosis.
      SIZE:770aminoacids;86943Da
      SUBUNIT:Binds,viaitsC-terminus,tothePIDdomainofseveralcytoplasmicproteins,includingAPBBfamilymembers,theAPBAfamily,MAPK8IP1,SHC1and,NumbandDab1(Bysimilarity).BindingtoDab1inhibitsitsserinephosphorylation(Bysimilarity).AlsointeractswithGPCR-likeproteinBPP,FPRL1,APPBP1,IB1,KNS2(viaitsTPRdomains)(Bysimilarity),APPBP2(viaBaSS)andDDB1.Invitro,itbindsMAPTviatheMT-bindingdomains(Bysimilarity).AssociateswithmicrotubulesinthepresenceofATPandinakinesin-dependentmanner(Bysimilarity).Interacts,throughaC-terminaldomain,withGNAO1.Amyloidbeta-42bindsCHRNA7inhippocampalneurons.Beta-amyloidassociateswithHADH2.SolubleAPPbinds,viaitsN-terminalhead,toFBLN1.InteractswithCPEB1(Bysimilarity).
      SUBCELLULARLOCATION:Membrane;Single-passtypeImembraneprotein.Note=Cellsurfaceproteinthatrapidlybecomesinternalizedviaclathrin-coatedpits.Duringmaturation,theimmatureAPP(N-glycosylatedintheendoplasmicreticulum)movestotheGolgicomplexwherecompletematurationoccurs(O-glycosylatedandsulfated).Afteralpha-secretasecleavage,solubleAPPisreleasedintotheextracellularspaceandtheC-terminalisinternalizedtoendosomesandlysosomes.SomeAPPaccumulatesinsecretorytransportvesiclesleavingthelateGolgicompartmentandreturnstothecellsurface.Gamma-CTF(59)peptideislocatedtoboththecytoplasmandnucleiofneurons.ItcanbetranslocatedtothenucleusthroughassociationwithFe65.Beta-APP42associateswithFRPL1atthecellsurfaceandthecomplexisthenrapidlyinternalized.APPsortstothebasolateralsurfaceinepithelialcells.Duringneuronaldifferentiation,theThr-743phosphorylatedformislocatedmainlyingrowthcones,moderatelyinneuritesandsparinglyinthecellbody.Caseinkinasephosphorylationcanoccureitheratthecellsurfaceorwithinapost-Golgicompartment.
      TISSUESPECIFICITY:Expressedinallfetaltissuesexaminedwithhighestlevelsinbrain,kidney,heartandspleen.Weakexpressioninliver.Inadultbrain,highestexpressionfoundinthefrontallobeofthecortexandintheanteriorperisylviancortex-operculargyri.Moderateexpressioninthecerebellarcortex,theposteriorperisylviancortex-operculargyriandthetemporalassociatedcortex.Weakexpressionfoundinthestriate,extra-striateandmotorcortices.IsoformAPP695isthepredominantforminneuronaltissue,isoformAPP751andisoformAPP770arewidelyexpressedinnon-neuronalcells.IsoformAPP751isthemostabundantforminT-lymphocytes.Appicanisexpressedinastrocytes.
      DOMAIN:SwissProt:P05067Thebasolateralsortingsignal(BaSS)isrequiredforsortingofmembraneproteinstothebasolateralsurfaceofepithelialcells.&TheNPXYsequencemotiffoundinmanytyrosine-phosphorylatedproteinsisrequiredforthespecificbindingofthePIDdomain.However,additionalaminoacidseitherN-orC-terminaltotheNPXYmotifareoftenrequiredforcompleteinteraction.ThePIDdomain-containingproteinswhichbindAPPrequiretheYENPTYmotifforfullinteraction.Theseinteractionsareindependentofphosphorylationontheterminaltyrosineresidue.TheNPXYsiteisalsoinvolvedinclathrin-mediatedendocytosis.
      PTM:Proteolyticallyprocessedundernormalcellularconditions.Cleavagebyalpha-secretaseoralternativelybybeta-secretaseleadstogenerationandextracellularreleaseofsolubleAPPpeptides,S-APP-alphaandS-APP-beta,respectively,andtheretentionofcorrespondingmembrane-anchoredC-terminalfragments,C83andC99.SubsequentprocessingofC83bygamma-secretaseyieldsP3peptides.Thisisthemajorsecretorypathwayandisnon-amyloidogenic.Alternatively,presenilin/nicastrin-mediatedgamma-secretaseprocessingofC99releasestheamyloidbetaproteins,amyloid-beta40(Abeta40)andamyloid-beta42(Abeta42),majorcomponentsofamyloidplaques,andthecytotoxicC-terminalfragments,gamma-CTF(50),gamma-CTF(57)andgamma-CTF(59).&Proteolyticallycleavedbycaspasesduringneuronalapoptosis.CleavageatAsp-739byeithercaspase-6,-8or-9resultsintheproductionoftheneurotoxicC31peptideandtheincreasedproductionofbeta-amyloidpeptides.&N-andO-glycosylated.O-linkageofchondroitinsulfatetotheL-APPisoformsproducestheAPPproteoglycancoreproteins,theappicans.Thechondroitinsulfatechainofappicanscontains4-O-sulfatedgalactoseinthelinkageregionandchondroitinsulfateEintherepeateddisaccharideregion(Bysimilarity).&PhosphorylationintheC-terminalontyrosine,threonineandserineresiduesisneuron-specific.PhosphorylationcanaffectAPPprocessing,neuronaldifferentiationandinteractionwithotherproteins.PhosphorylatedonThr-743inneuronalcellsbyCdc5kinaseandMapk10,individingcellsbyCdc2kinaseinacell-cycledependentmannerwithmaximallevelsattheG2/Mphaseand,invitro,byGSK-3-beta.TheThr-743phosphorylatedformcausesaconformationalchangewhichreducesbindingofFe65familymembers.PhosphorylationonTyr-757isrequiredforSHCbinding.Phosphorylatedintheextracellulardomainbycaseinkinasesonbothsolubleandmembrane-boundAPP.Thisphosphorylationisinhibitedbyheparin.&Extracellularbindingandreductionofcopper,resultsinacorrespondingoxidationofCys-144andCys-158,andtheformationofadisulfidebond.Invitro,theAPP-Cu(+)complexinthepresenceofhydrogenperoxideresultsinanincreasedproductionofbeta-amyloid-containingpeptides.
      DISEASE:SwissProt:P05067#DefectsinAPPareacauseofautosomaldominantAlzheimerdisease(AD)[MIM:104300].ADisthemostprevelantformofdementia,characterizedbyneurofibrillarytanglesandamyloidplaquesdepositioninthebrain.IdenticallesionsoccurintheneuronsofagedDownsyndromebutatanearlieragethaninAD.Themajorconstituentoftheseneuriticplaquesistheneurotoxicamyloid-beta-APP40-42peptide(s),derivedproteolyticallyfromthetransmembraneprecursorproteinAPPbysequentialsecretaseprocessing.Mutationsoccurringatthebeta-amyloidN-terminal,suchastheSwedishdoublemutation,appeartoincreaselevelsofbeta-amyloidbyfacilitatingbeta-secretasecleavageresultinginelevatedlevelsofbothbeta-APP42andbeta-APP40.ThecytotoxicC-terminalfragments(CTFs)andthecaspase-cleavedproductssuchasC31,arealsoimplicatedinADneuronaldeath.AlzheimerdiseasecausedbymutationsinAPPisarareoccurrenceandusuallycausesthefamilialorearly-onsetformofthedisease(FAD).Flemish-typeADischaracterizedby,inadditiontopreseniledementia,cerebralhemorrhagingduetocerebralamyloidangiopathywhichissimilarto,butdistinctfrom,cerebroarterialamyloidosisDutchtype.Onlyabout5%ofallcasesofAlzheimerdiseasearecausedbyFADmutations,therestaresporADIc.&DefectsinAPParethecauseofhereditarycerebralhemorrhagewithamyloidosisDutchtype(HCHWAD)[MIM:609065].HCHWADischaracterizedbyamyloiddepositsincerebralvessels.Theprincipalclinicalcharacteristicsarerecurringcerebralhemorrhages,sometimesprecededbymigrainousheadachesormentalcleavage.Beta-APP40isthepredominantformofcerebrovascularamyloid.&DefectsinAPParethecauseofhereditarycerebroarterialamyloidosisIowatype[MIM:605714].HereditarycerebroarterialamyloidosisIowatypeisanautosomaldominantdementiabeginninginthesixthorseventhdecadeoflife.Thepatientshaveprogressiveaphasicdementia,leukoencephalopathy,andoccipitalcalcifications.Theydonotpresentcerebralhemorrhaging.
      SIMILARITY:BelongstotheAPPfamily.&Contains1BPTI/Kunitzinhibitordomain.
      MISCELLANEOUS:Chelationofmetalions,notablycopper,ironandzinc,caninducehistidine-bridgingbetweenbeta-amyloidmoleculesresultinginbeta-amyloid-metalaggregates.Theaffinityforcopperismuchhigherthanforothertransientmetalsandisincreasedunderacidicconditions.Extracellularzinc-bindingincreasesbindingofheparintoAPPandinhibitscollagen-binding.
      PhysicochemicalInformation
      Dimensions
      MaterialsInformation
      MaterialsInformation
    售后保障
    螞蟻淘生物188，秉承螞蟻淘一貫的嚴謹態(tài)度，由螞蟻淘公司專業(yè)人員負責品控、采購、物流、銷售、售后，保障正品優(yōu)質(zhì)。以“快速好省，為科研提供好產(chǎn)品、好價格”為理念，直接鏈接原廠家，從全國各地原制造商嚴格挑選188款科研精品，剔除品牌溢價，188生物新電商，把好的產(chǎn)品帶給科研！? 力求給你最優(yōu)質(zhì)的商品。
  • Q：生物188產(chǎn)品正品保障嗎？
    A：生物188質(zhì)量把控人員具有十年的從業(yè)經(jīng)驗，在業(yè)界享有良好的口碑；自營商城，直接從廠家采購， 自己的團隊負責國際物流和清關，中間沒有第三方，所有流程嚴格把控，100%保證正品，假一罰十。

    Q：下單后可以修改訂單嗎？
    A：下單后的商品付款之前可以修改；訂單付款成功，需要聯(lián)系我們客服進行修改；客服電話：4000-520-616

    Q：可以開發(fā)票嗎？
    A：本網(wǎng)站所售商品都是正規(guī)清關，均開具16%正規(guī)發(fā)票，發(fā)票金額含配送費金額，另有說明的除外。

    Q：商品幾天可以發(fā)貨？
    A：生物188商品，全部現(xiàn)貨銷售，付款后即可發(fā)貨,一般一周內(nèi)送達！

    Q：如何聯(lián)系商家？
    A：有任何問題夠可以電話咨詢我們，全國24小時免費服務熱線：4000-520-616 或聯(lián)系我們的在線客服QQ：1570468124

    Q：收到的商品少了/發(fā)錯了怎么辦？
    A：同個訂單購買多個商品可能會分為一個以上包裹發(fā)出，可能不會同時送達，建議查看訂單詳情是否是 部分發(fā)貨狀態(tài)；如未收到，可聯(lián)系在線客服或者致電4000-520-616。

    Q：退換貨/維修需要多長時間？
    A：一般情況下，退貨處理周期為客戶收到產(chǎn)品一個月內(nèi)（以快遞公司顯示簽收時間為準），包裝規(guī)格、 數(shù)量、品種不符，外觀毀損、短缺或缺陷，請在收到貨24小時內(nèi)申請退換貨；特殊商品以合同條款為準。

何為188

極簡而嚴謹，我們僅銷售188款生物醫(yī)學科研用品，款款都是爆款；因為少所以聚焦，聚焦甄選每一款產(chǎn)品，聚焦服務每一位客戶!

關注我們 :

點擊QQ聯(lián)系我們
生物188微信

關注188微信公眾號

獲取最新優(yōu)惠活動通知

  • 品質(zhì)甄選，正品保證

  • 自營電商，廠家直采

  • 極簡主義，188精品