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Millipore/06-1283 | Anti-acetyl-p53 (Lys320) Antibody/06-1283/100 µg
  • Millipore/06-1283 | Anti-acetyl-p53 (Lys320) Antibody/06-1283/100 µg

Millipore/06-1283 | Anti-acetyl-p53 (Lys320) Antibody/06-1283/100 µg

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貨號(hào): 06-1283
品牌: Millipore
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    • Description
      CatalogueNumber06-1283
      Replaces06-915
      DescriptionAnti-acetyl-p53(Lys320)Antibody
      AlternateNames
      • AntigenNY-CO-13
      • Phosphoproteinp53
      • Tumorsuppressorp53
      • p53antigen
      • p53transformationsuppressor
      • p53tumorsuppressor
      • transformation-relatedprotein53
      • tumorproteinp53
      BackgroundInformationp53wasdiscoveredin1979asacellularproteinassociatingwiththetransformingproteinofSV40tumorvirus.Sincethen,manydifferentbiochemicalfunctionshavebeenattributedtothe53kDphosphoprotein.Experimentalevidencehassuggestedthatp53actsasanegativeregulatorofcellgrowthinnormalcells(Finlay,1989).Thus,theinactivationormutationofp53maybeanessentialstepinthedevelopmentofmalignancy(LaneandBenchmol,1990).Wild-typep53levelsinnormalcellsandtissueswerefoundtobeverylow.Mutantp53polypeptide,however,isoftenfoundtobepresentathighconcentrationsinmammaliantumorsandtumorcelllines.Forexample,inanimmuno-histochemistrystudy40%ofhumanbreastcancershowedelevatedlevelsofmutantp53inthecellnucleus.Mutationsofthep53proteinhavesomecharacteristicfeatures:
      a)Mostofthemaremissensepointmutationsgivingrisetoanalteredproteinfunction.
      b)Many-butnotall-mutantp53proteinsexhibitacommonmutantstructure,whichcanberecognizedbymonoclonalantibodiesspecificforp53inthemutantconformation.
      ProductInformation
      FormatAffinityPurified
      Control
      • Recombinantproteins
      PresentationPurifiedrabbitpolyclonalinbuffercontaining0.1MTris-Glycine(pH7.4),150mMNaClwith0.05%sodiumazide.
      StorageandShippingInformation
      StorageConditionsStablefor1yearat2-8°Cfromdateofreceipt.
      Applications
      ApplicationUseAnti-acetyl-p53(Lys320)Antibody(RabbitPolyclonalAntibody)validatedinWBtodetectacetyl-p53(Lys320)alsoknownasAntigenNY-CO-13,Phosphoproteinp53,Tumorsuppressorp53,p53antigen.
      KeyApplications
      • WesternBlotting
      ApplicationNotesWesternBlotAnalysis:5μg/mLantibodydetectedp53on10μgofA549cellstreatedwithUV&TSAlysate.

      WesternBlot(SNAPID)Analysis:5μg/mLantibodydetectedp53on10μgofrecombinantproteins.
      BIOLOGicalInformation
      ImmunogenKLH-conjugatedlinearpeptidecorrespondingtop53atLys320.
      EpitopeAcetylLys320
      ConcentrationPleaserefertotheCertificateofAnalysisforthelot-specificconcentration.
      HostRabbit
      SpecificityThisantibodyrecognizesp53acetylatedatLys320.
      SpeciesReactivity
      • Human
      • Chimpanzee
      • Bovine
      SpeciesReactivityNoteDemonstratedtoreactwithhuman.Predictedtoreactwithchimpanzeeandbovinebasedon100%sequencehomology.
      AntibodyTypePolyclonalAntibody
      EntrezGeneNumber
      EntrezGeneSummaryThisgeneencodestumorproteinp53,whichrespondstodiversecellularstressestoregulatetargetgenesthatinducecellcyclearrest,apoptosis,senescence,DNArepair,orchangesinmetabolism.p53proteinisexpressedatlowlevelinnormalcellsandatahighlevelinavarietyoftransformedcelllines,whereit"sbelievedtocontributetotransformationandmalignancy.p53isaDNA-bindingproteincontainingtranscriptionactivation,DNA-binding,andoligomerizationdomains.Itispostulatedtobindtoap53-bindingsiteandactivateexpressionofdownstreamgenesthatinhibitgrowthand/orinvasion,andthusfunctionasatumorsuppressor.Mutantsofp53thatfrequentlyoccurinanumberofdifferenthumancancersfailtobindtheconsensusDNAbindingsite,andhencecausethelossoftumorsuppressoractivity.Alterationsofthisgeneoccurnotonlyassomaticmutationsinhumanmalignancies,butalsoasgermlinemutationsinsomecancer-pronefamilieswithLi-Fraumenisyndrome.Multiplep53variantsduetoalternativepromotersandmultiplealternativesplicinghavebeenfound.Thesevariantsencodedistinctisoforms,whichcanregulatep53transcriptionalactivity.[providedbyRefSeq].
      GeneSymbol
      • LFS1
      • P53
      • TRP53
      • p53
      PurificationMethodAffinityPurfied
      UniProtNumber
      UniProtSummaryFUNCTION:Actsasatumorsuppressorinmanytumortypes;inducesgrowtharrestorapoptosisdependingonthephysiologicalcircumstancesandcelltype.Involvedincellcycleregulationasatrans-activatorthatactstonegativelyregulatecelldivisionbycontrollingasetofgenesrequiredforthisprocess.Oneoftheactivatedgenesisaninhibitorofcyclin-dependentkinases.ApoptosisinductionseemstobemediatedeitherbystimulationofBAXandFASantigenexpression,orbyrepressionofBcl-2expression.ImplicatedinNotchsignalingcross-over.

      CofactorBinds1zincionpersubunit.

      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.InteractswithPPP2R.

      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].

      SEQUENCESIMILARITIES:Belongstothep53family.
      MolecularWeight~53kDaobserved.WesternBlotofA549cellstreatedwithUV&TSAshowbandsat~48kDaand~14kDawhicharelikelybreakdownproductsofp53reportedforUVtreatedcells.(Sadji-Ouatas,2002)
      PhysicochemicalInformation
      Dimensions
      MaterialsInformation
      MaterialsInformation
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