商品介绍
| Description | |
|---|---|
| CatalogueNumber | MAB5228 |
| BrandFamily | Chemicon® |
| TradeName |
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| Description | Anti-AmyloidPrecursorProteinAntibody,Secretory,cloneOM84 |
| AlternateNames |
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| ProductInformation | |
|---|---|
| Format | Purified |
| Control |
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| Presentation | ProteinAPurifiedmouseimmunoglobulinin10mMsodiumphosphatebuffer(pH7.4),0.15MNaCl,and0.1%sodiumazideasapreservative.. |
| StorageandShippingInformation | |
|---|---|
| StorageConditions | Maintainfrozenat-70°Corbelowinundilutedaliquotsforupto12months,avoidrepeatedfreeze/thawcycles. |
| Applications | |
|---|---|
| Application | Anti-AmyloidPrecursorProteinAntibody,Secretory,cloneOM84detectslevelofAmyloidPrecursorProtein&hasbeenpublished&validatedforuseinELISA&WB. |
| KeyApplications |
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| ApplicationNotes | Westernblot:10μg/mLELISA:1μg/mL Optimalworkingdilutionsmustbedeterminedbyenduser. |
| BIOLOGicalInformation | |
|---|---|
| Immunogen | AmyloidPrecursorProtein(APP)secretedbytheEJ-1bladdercarcinomacellline. |
| Epitope | Secretory |
| Clone | OM84 |
| Concentration | PleaserefertotheCertificateofAnalysisforthelot-specificconcentration. |
| Host | Mouse |
| Specificity | Reactswithsecretoryamyloidprecursorprotein(sAPP),butnotwithAmyloid-Betaprotein1-40. |
| Isotype | IgG2aκ |
| SpeciesReactivity |
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| AntibodyType | MonoclonalAntibody |
| EntrezGeneNumber | |
| EntrezGeneSummary | Thisgeneencodesacellsurfacereceptorandtransmembraneprecursorproteinthatiscleavedbysecretasestoformanumberofpeptides.SomeofthesepeptidesaresecretedandcanbindtotheacetyltransferasecomplexAPBB1/TIP60topromotetranscriptionalactivation,whileothersformtheproteinbasisoftheamyloidplaquesfoundinthebrainsofpatientswithAlzheimerdisease.MutationsinthisgenehavebeenimplicatedinautosomaldominantAlzheimerdiseaseandcerebroarterialamyloidosis(cerebralamyloidangiopathy).Multipletranscriptvariantsencodingseveraldifferentisoformshavebeenfoundforthisgene. |
| GeneSymbol |
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| PurificationMethod | ProteinAPurfied |
| UniProtNumber | |
| UniProtSummary | FUNCTION: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. |
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| Millipore/475855-1R神奇滤布 密理博Millipore现货促销 | 475855-1R | Life Science Research | 膜 | 93.50 | Millipore/17-701/EZ-Magna RIP™ RNA-Binding Protein Immunoprecipitation Kit | 17-701 | Life Science Research | 定量试剂盒 | 653.00 | Millipore/RIPAb+ Ago2 - RIP Validated Antibody and Primer Set | 03-110 | Life Science Research | 抗体套装 | 433.00 | Millipore/CBL468F | Anti-PECAM-1 Antibody, clone HC1/6, FITC conjugated/CBL468F/100 assays | CBL468F | Antibodies and Assays | 功能性抗体 | 298.00 | Millipore/ECM460 | αVβ3/PECAM Investigator Kit/ECM460/1 kit | ECM460 | Antibodies and Assays | 夹心法ELISA | 477.00 |
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