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Millipore/04-1146 | Anti-acetyl-p53 (Lys382) Antibody, clone EPR358(2), rabbit monoclonal/04-1146/100 µL
  • Millipore/04-1146 | Anti-acetyl-p53 (Lys382) Antibody, clone EPR358(2), rabbit monoclonal/04-1146/100 µL

Millipore/04-1146 | Anti-acetyl-p53 (Lys382) Antibody, clone EPR358(2), rabbit monoclonal/04-1146/100 µL

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貨號: 04-1146
品牌: Millipore
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    • Description
      CatalogueNumber04-1146
      DescriptionAnti-acetyl-p53(Lys382)Antibody,cloneEPR358(2),rabbitmonoclonal
      AlternateNames
      • AntigenNY-CO-13
      • Phosphoproteinp53
      • Tumorsuppressorp53
      • p53antigen
      • p53transformationsuppressor
      • p53tumorsuppressor
      • transformation-relatedprotein53
      • tumorproteinp53
      BackgroundInformationp53wasdiscoveredin1979asacellularproteinassociatingwiththetransformingproteinofSV40tumorvirus.Sincethen,manydifferentbiochemicalfunctionshavebeenattributedtothe53kDphosphoprotein.Experimentalevidencehassuggestedthatp53actsasanegativeregulatorofcellgrowthinnormalcells.Thus,theinactivationormutationofp53maybeanessentialstepinthedevelopmentofmalignancy.Wild-typep53levelsinnormalcellsandtissueswerefoundtobeverylow.Mutantp53polypeptide,however,isoftenfoundtobepresentathighconcentrationsinmammaliantumorsandtumorcelllines.Forexample,inanimmuno-histochemistrystudy40%ofhumanbreastcancershowedelevatedlevelsofmutantp53inthecellnucleus.Mutationsofthep53proteinhavesomecharacteristicfeatures:
      a)Mostofthemaremissensepointmutationsgivingrisetoanalteredproteinfunction.
      b)Many-butnotall-mutantp53proteinsexhibitacommonmutantstructure,whichcanberecognizedbymonoclonalantibodiesspecificforp53inthemutantconformation.
      ProductInformation
      FormatUnpurified
      Control
      • HepG2celllysate
      PresentationRabbitMonoclonalinbuffercontaining50mMTris-Glycine(pH7.4),0.15MNaClcontaining40%Glycerol,0.01%sodiumazideand0.05%BSA.
      StorageandShippingInformation
      StorageConditionsStablefor1yearat-20oCfromdateofreceipt.
      HandlingRecommendations:Uponfirstthaw,andpriortoremovingthecap,centrifugethevialandgentlymixthesolution.Aliquotintomicrocentrifugetubesandstoreat-20°C.Avoidrepeatedfreeze/thawcycles,whichmaydamageIgGandaffectproductperformance.Note:VariABIlityinfreezertemperaturesbelow-20°Cmaycauseglycerolcontainingsolutionstobecomefrozenduringstorage.
      Applications
      ApplicationAnti-acetyl-p53(Lys382)Antibody,cloneEPR358(2)isaRabbitMonoclonalAntibodyfordetectionofacetyl-p53(Lys382)alsoknownasTumorsuppressorp53,p53antigen&hasbeenvalidatedinWB,ICC.
      KeyApplications
      • WesternBlotting
      • Immunocytochemistry
      ApplicationNotesImmunocytochemistryAnalysis:A1:100dilutionfromapreviouslotwasusedinIC.
      BIOLOGicalInformation
      ImmunogenAcetylatedsyntheticpeptidecorrespondingtoresiduessurroundingLys382ofhumanp53.
      EpitopeAcetylatedLys382
      CloneEPR358(2)
      HostRabbit
      SpecificityThisantibodyonlydetectsp53acetylatedonLys382.
      IsotypeIgG
      SpeciesReactivity
      • Human
      AntibodyTypeMonoclonalAntibody
      EntrezGeneNumber
      GeneSymbol
      • FLJ92943
      • LFS1
      • P53
      • TRP53
      • p53
      Modifications
      • Acetylation
      PurificationMethodUnpurified
      UniProtNumber
      UniProtSummaryFUNCTION:Actsasatumorsuppressorinmanytumortypes;inducesgrowtharrestorapoptosisdependingonthephysiologicalcircumstancesandcelltype.Involvedincellcycleregulationasatrans-activatorthatactstonegativelyregulatecelldivisionbycontrollingasetofgenesrequiredforthisprocess.Oneoftheactivatedgenesisaninhibitorofcyclin-dependentkinases.ApoptosisinductionseemstobemediatedeitherbystimulationofBAXandFASantigenexpression,orbyrepressionofBcl-2expression.ImplicatedinNotchsignalingcross-over.
      COFACTOR:Binds1zincionpersubunit.
      SUBUNITSTRUCTURE:InteractswithAXIN1.ProbablypartofacomplexconsistingofTP53,HIPK2andAXIN1Bysimilarity.BindsDNAasahomotetramer.InteractswithhistoneacetyltransferasesEP300andmethyltransferasesHRMT1L2andCARM1,andrecruitsthemtopromoters.Invitro,theinteractionofTP53withcancer-associated/HPV(E6)viralproteinsleadstoubiquitinationanddegradationofTP53givingapossIBLemodelforcellgrowthregulation.Thiscomplexformationrequiresanadditionalfactor,E6-AP,whichstablyassociateswithTP53inthepresenceofE6.Interacts(viaC-terminus)withTAF1;whenTAF1ispartoftheTFIIDcomplex.InteractswithING4;thisinteractionmaybeindirect.FoundinacomplexwithCABLES1andTP73.InteractswithHIPK1,HIPK2,andP53DINP1.InteractswithWWOX.MayinteractwithHCVcoreprotein.InteractswithUSP7andSYVN1.InteractswithHSP90AB1.InteractswithCHD8;leADIngtorecruithistoneH1andpreventtransactivationactivityBysimilarity.InteractswithARMC10,BANP,CDKN2AIPandE4F1.InteractswithYWHAZ;theinteractionenhancesTP53transcriptionalactivity.PhosphorylationofYWHAZon"Ser-58"inhibitsthisinteraction.Interacts(viaDNA-bindingdomain)withMAML1(viaN-terminus).InteractswithMKRN1.DirectlyinteractswithFBXO42;leadingtoubiquinationanddegradationofTP53.Interacts(phosphorylatedatSer-15byATM)withthephosphatasePP2A-PPP2R5Choloenzyme;regulatesstress-inducedTP53-dependentinhibitionofcellproliferation.InteractswithPPP2R2A.
      SUBCELLULARLOCATION:Cytoplasm.Nucleus.Endoplasmicreticulum.Note:InteractionwithBANPpromotesnuclearlocalization.
      DOMAIN:Thenuclearexportsignalactsasatranscriptionalrepressiondomain.
      PTM:Acetylated.AcetylationofLys-382byCREBBPenhancestranscriptionalactivity.DeacetylationofLys-382bySIRT1impairsitsabilitytoinduceproapoptoticprogramandmodulatecellsenescence.
      PhosphorylationonSerresiduesmediatestranscriptionalactivation.PhosphorylatedbyHIPK1Bysimilarity.PhosphorylationatSer-9byHIPK4increasesrepressionactivityonBIRC5promoter.PhosphorylatedonThr-18byVRK1,whichmaypreventtheinteractionwithMDM2.PhosphorylatedonThr-55byTAF1,whichpromotesMDM2-mediateddegradation.PhosphorylatedonSer-46byHIPK2uponUVirradiation.PhosphorylationonSer-46isrequiredforacetylationbyCREBBP.PhosphorylatedonSer-392followingUVbutnotgammairradiation.PhosphorylateduponDNAdamage,probablybyATMorATR.PhosphorylatedonSer-15uponultravioletirradiation;whichisenhancedbyinteractionwithBANP.
      DephosphorylatedbyPP2A-PPP2R5CholoenzymeatThr-55.SV40smallTantigeninhibitsthedephosphorylationbytheACformofPP2A.
      MaybeO-glycosylatedintheC-terminalbasicregion.StudiedinEB-1cellline.
      UbiquitinatedbySYVN1,whichleadstoproteasomaldegradation.UbiquitinatedbyMKRN1atLys-291andLys-292,whichleadstoproteasomaldegradation.
      MonomethylatedatLys-372bySETD7,leadingtostabilizationandincreasedtranscriptionalactivation.MonomethylatedatLys-370bySMYD2,leadingtodecreasedDNA-bindingactivityandsubsequenttranscriptionalregulationactivity.Lys-372monomethylationpreventsinteractionwithSMYD2andsubsequentmonomethylationatLys-370.
      SumoylatedbySUMO1.
      Demethylationofdi-methylatedLys-370byKDM1/LSD1preventsinteractionwithTP53BP1andrepressesTP53-mediatedtranscriptionalactivation.
      INVOLVEMENTINDISEASE:TP53isfoundinincreasedamountsinawidevarietyoftransformedcells.TP53isfrequentlymutatedorinactivatedinabout60%ofcancers.
      DefectsinTP53areinvolvedinesophagealsquamouscellcarcinoma(ESCC)[MIM:133239].ESCCisatumoroftheesophagus.
      DefectsinTP53areacauseofLi-Fraumenisyndrome(LFS)[MIM:151623].LFSisanautosomaldominantfamilialcancersyndromethatinitsclassicformisdefinedbytheexistenceofaprobandaffectedbyasarcomabefore45yearswithafirstdegreerelativeaffectedbyanytumorbefore45yearsandanotherfirstdegreerelativewithanytumorbefore45yearsorasarcomaatanyage.OtherclinicaldefinitionsforLFShavebeenproposed(Ref.107andRef.110)andcalledLi-Fraumenilikesyndrome(LFL).Inthesefamiliesaffectedrelativesdevelopadiversesetofmalignanciesatunusuallyearlyages.Fourtypesofcancersaccountfor80%oftumorsoccurringinTP53germlinemutationcarriers:breastcancers,softtissueandbonesarcomas,braintumors(astrocytomas)andadrenocorticalcarcinomas.Lessfrequenttumorsincludechoroidplexuscarcinomaorpapillomabeforetheageof15,rhaBDomyosarcomabeforetheageof5,leukemia,Wilmstumor,malignantphyllodestumor,colorectalandgastriccancers.
      DefectsinTP53maybeassociatedwithnasopharyngealcarcinoma[MIM:161550];alsoknownasnasopharyngealcancer.
      DefectsinTP53arefoundinBarrettmetaplasia;alsoknownasBarrettesophagus.Itisaconditioninwhichthenormallystratifiedsquamousepitheliumoftheloweresophagusisreplacedbyametaplasticcolumnarepithelium.Theconditiondevelopsasacomplicationinapproximately10%ofpatientswithchronicgastroesophagealrefluxdiseaseandpredisposestothedevelopmentofesophagealadenocarcinoma.
      DefectsinTP53areinvolvedinheadandnecksquamouscellcarcinomas(HNSCC)[MIM:275355];alsoknownassquamouscellcarcinomaoftheheadandneck.
      DefectsinTP53areinvolvedinoralsquamouscellcarcinoma(OSCC).Cigarettesmokeisaprimemutagenicagentincanceroftheaerodigestivetract.
      DefectsinTP53areacauseoflungcancer[MIM:211980].
      DefectsinTP53areacauseofchoroidplexuspapilloma[MIM:260500].Choroidplexuspapillomaisaslow-growingbenigntumorofthechoroidplexusthatofteninvadestheleptomeninges.Inchildrenitisusuallyinalateralventriclebutinadultsitismoreofteninthefourthventricle.Hydrocephalusiscommon,eitherfromobstructionorfromtumorsecretionofcerebrospinalfluid.Ifitundergoesmalignanttransformationitiscalledachoroidplexuscarcinoma.Primarychoroidplexustumorsarerareandusuallyoccurinearlychildhood.
      DefectsinTP53areacauseofoneformofhereditaryadrenocorticalcarcinoma(ADCC)[MIM:202300].ADCCisararechildhoodtumor,representingabout0.4%ofchildhoodtumors,withahighincidenceofassociatedtumors.ADCCoccurswithincreasedfrequencyinpatientswiththeBeckwith-Wiedemannsyndrome[MIM:130650]andisacomponenttumorinLi-Fraumenisyndrome[MIM:151623].
      SEQEUNCESIMILARITIES:Belongstothep53family.
      MolecularWeight~53kDa
      PhysicochemicalInformation
      Dimensions
      MaterialsInformation
      MaterialsInformation
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