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Millipore/AB9985 | Anti-glutathione p53 (Cys141) Antibody/AB9985/100 µL
  • Millipore/AB9985 | Anti-glutathione p53 (Cys141) Antibody/AB9985/100 µL

Millipore/AB9985 | Anti-glutathione p53 (Cys141) Antibody/AB9985/100 µL

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貨號: AB9985
品牌: Millipore
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    • Description
      CatalogueNumberAB9985
      DescriptionAnti-glutathionep53(Cys141)Antibody
      AlternateNames
      • AntigenNY-CO-13
      • Phosphoproteinp53
      • Tumorsuppressorp53
      • p53antigen
      • p53transformationsuppressor
      • p53tumorsuppressor
      • transformation-relatedprotein53
      • tumorproteinp53
      BackgroundInformationCellulartumorantigenp53isamemberofthep53familyandisfoundinthecytoplasm,nucleus,andendoplasmicreticulum.Itfunctionsasatumorsuppressorwithinavarietyoftumorsbyeitherstimulatingapoptosisorgrowtharrestindeferencetocelltypeandphysiologicalfactors.p53servesasatrans-activator,negativelyregulatingcelldivisionduringcellcycleregulation.Itisalsothoughttobeinvolvedinthecross-overforNotchsignaling.Defectsinp53expressionhavebeenimplicatedinseveraldiseasesincluding;choroidplexuspapilloma,lungcancer,head/necksquamouscellcarcinomas,esophagealsquamouscellcarcinoma,Li-Fraumenisyndrome,andhereditaryadrenocortivalcarcinoma.Mutationsofthep53proteinhavesomecharacteristicfeatures:a)Mostofthemaremissensepointmutationsgivingrisetoanalteredproteinfunction,andb)Many-butnotall-mutantp53proteinsexhibitacommonmutantstructure,whichcanberecognizedbymonoclonalantibodiesspecificforp53inthemutantconformation.
      ProductInformation
      FormatAffinityPurified
      Control
      • Prostateadenocarcinomatissue
      PresentationPurifiedrabbitpolyclonalinbuffercontaining0.1MTris-Glycine(pH7.4),150mMNaClwith0.05%sodiumazide.
      StorageandShippingInformation
      StorageConditionsStablefor1yearat2-8°Cfromdateofreceipt.
      Applications
      ApplicationAnti-glutathionep53(Cys141)Antibodyisarabbitpolyclonalantibodyfordetectionofglutathionep53(Cys141)alsoknownasAntigenNY-CO-13,Phosphoproteinp53,Tumorsuppressorp53&hasbeenvalidatedinWB,IP,IHC,ICC.
      KeyApplications
      • WesternBlotting
      • Immunoprecipitation
      • Immunohistochemistry
      • Immunocytochemistry
      ApplicationNotesWesternBlotAnalysis:ArepresentativelotwasusedbyanindependentlaboratoryinWB.(Dr.KalkunteS.Srivenugopal,DepartmentofBiomedicalSciences,TexasTechUniversityHealthSciencesCenter,1406S.Coulter,Amarillo,TX79106.)

      ImmunoprecipitationAnalysis:ArepresentativelotwasusedbyanindependentlaboratoryinIP.(Yusef,M,etal.(2010).FreeRADIcBiolMed.49(5):908-917.)

      ImmunocytochemistryAnalysis:ArepresentativelotwasusedbyanindependentlaboratoryinIC.(Yusef,M,etal.(2010).FreeRadicBiolMed.49(5):908-917.)
      BIOLOGicalInformation
      ImmunogenKLH-conjugatedlinearpeptidecorrespondingtohumanp53glutathionylatedatCys141.
      Epitopep53glutathionylatedatCys141
      ConcentrationPleaserefertotheCertificateofAnalysisforthelot-specificconcentration.
      HostRabbit
      SpecificityThisantibodyrecognizesp53whenglutathionylatedatCys141.
      SpeciesReactivity
      • Human
      • Chimpanzee
      • RhesusMacaque
      • GroundSquirrel
      • Monkey
      • Hamster
      SpeciesReactivityNoteDemonstratedtoreactwithhuman.
      Predictedtoreactwithchimpanzee,rhesusmacaque,groundsquirrel,monkey,hamster,commonmarmoset,rabbit,andorangutanbasedon100%sequencehomology.
      Otherhomologies:Rat(92%sequencehomology).Mouse(85%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
      Modifications
      • Glutathionylation
      PurificationMethodAffinityPurfied
      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.

      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.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.103andRef.106)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].

      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
      PhysicochemicalInformation
      Dimensions
      MaterialsInformation
      MaterialsInformation
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