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Millipore/17-475 | Phospho-p53 (Ser15) STAR ELISA Kit/17-475/96 assays
Millipore/17-475 | Phospho-p53 (Ser15) STAR ELISA Kit/17-475/96 assays
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¥0.00
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0.00
产品分类：
夹心法ELISA
公司分类：
Sandwich_method_ELISA
联系Q Q：
3392242852
电话号码：
4000-520-616
电子邮箱：
info@ebiomall.com
商品介绍
| Description | |
|---|---|
| CatalogueNumber | 17-475 |
| BrandFamily | Upstate |
| TradeName |
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| Description | Phospho-p53(Ser15)STARELISAKit |
| BackgroundInformation | I.TESTPRINCIPLE ThecolorimetricSTAR(SignalTransductionAssayReaction)ELISAkitisasolidphasesandwichenzymelinkedimmunosorbentassaythatprovidesafast,sensitivemethodtodetectspecificlevelsofsignalingtargetsinwholecellextracts.Thep53plateiscoatedwithaspecificmousemonoclonalp53captureantibodyonthemicrowellsofthe96-wellclearplate.Samplelysateorthestandardincludedinthekitareincubatedinthemicrowellsallowingp53antigentobecapturedintheplatewells.Theplateisthenwashedtoremoveanyunboundnon-specificmaterial.Thewellsarethenincubatedwithaspecificrabbitanti-phospho-p53(Ser15)antibodytodetectthecapturedp53ontheplatewellthatisphosphorylatedonSer15.TheunbounddetectionantibodyiswashedawayfollowedbyincubationwithanHRP-conjugatedanti-rabbitantibody.AftertheadditionofTMBsubstrateandstopsolutiontheabsorbanceismeasuredat450nmusingaplatereader.Thisallowsforasensitiveenzymaticdetectionofthesample. Theentireassaytakeslessthan5hourstocompletewithminimalhands-ontime.Manyofthereagentsaresuppliedinready-touseformulationsforeaseofuse.Thekitalsoincludesastandardthatisrunasbothapositivecontrolandtogenerateastandardcurveforphosphorylatedp53(Ser15)measurement. II.p53BACKGROUND p53,agenethatismutatedinapproximatelyhalfofallhumancancers,haslongbeenregardedastheguardianofthegenomebyregulatinggenescontrollingcellcycleprogression,DNArepairandapoptosis.Inresponsetocellularstress,suchasDNAdamage,hypoxia,orrADIation,p53isactivatedandinturnittranscriptionallyactivatestheexpressionofparticulargenes,includingthecyclin-dependentkinaseinhibitorp21,andtogetherwithp19ARF,inducesexpressionofp21Cip1,tocausecellcyclearrest.Alternatively,p53canworkviaapoptosisasawayofeliminatingirreparablydamagedcells. Inactivationorlossofp53hasbeenassociatedwithderegulationofthecellcycleandDNAreplication,inefficientDNArepair,lossofcellularapoptoticresponsesandultimatelythedevelopmentofvarioushumancancers.Thep53polypeptidecontainsthreedistinctregions.Theamino-terminal83aminoacidsofp53containsthetransactivationdomain,aswellastheregioninvolvedintranscription-independentgrowthsuppression,thecentralsequence-specificDNAbindingregion,andthecarboxy-terminalregioncontainstheDNA-bindingdomain.ActivationandstABIlizationofp53isregulatedbyphosphorylationandpossIBLyacetylation |
| MaterialsRequiredbutNotDelivered | 1.Multi-channelorrepeatingPipettes 2.Plateshaker(optional) 3.Pipettorsandtipscapableofaccuratelymeasuring1-1000µL 4.GraduatedSEROlogicalpipettes 5.96-wellmicrotiterPlateReaderwith450nmfilter 6.Graphingsoftwareforplottingdataorgraphpaperformanualplottingofdata 7.Microfugetubesforstandardandsampledilutions 8.Mechanicalvortex 9.1litercontainer 10.Distilledordeionizedwater |
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| Detectionmethod | Colorimetric |
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| StorageConditions | Maintaintheunopenedkitat2-8°Cuntilexpirationdate. Precautions •Theinstructionsprovidedhavebeendesignedtooptimizethekit"sperformance.Deviationfromtheinstructionsmayresultinsuboptimalperformanceofthekitandthefailuretoproduceaccuratedata. •CausticMaterial:StopSolution.Caution:Eye,hand,face,andclothingprotectionshouldbewornwhenhandlingthismaterial. •SafetyWarningsandPrecautions:Thiskitisdesignedforresearchuseonlyandnotrecommendedforinternaluseinhumansoranimals.Allchemicalsshouldbeconsideredpotentiallyhazardousandprinciplesofgoodlaboratorypracticeshouldbefollowed. •TheDetectionAntibodyandELISADiluentcontainsodiumazide.Sodiumazidemayreactwithcopperandleadplumbingtoformhighlyexplosivemetalazides.Upondisposal,flushwithlargeamountsofwatertopreventazidebuild-up.Avoidcontactwithskin. •TheAnti-RabbitIgGHRPConjugateandHRPDiluentcontainthimerosal.Thimerosalishighlytoxicbyinhalation,contactwithskinorifswallowed.Thimerosalisapossiblemutagenandshouldbehandledaccordingly. |
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| EntrezGeneNumber | |
| EntrezGeneSummary | Tumorproteinp53,anuclearprotein,playsanessentialroleintheregulationofcellcycle,specificallyinthetransitionfromG0toG1.Itisfoundinverylowlevelsinnormalcells,however,inavarietyoftransformedcelllines,itisexpressedinhighamounts,andbelievedtocontributetotransformationandmalignancy.p53isaDNA-bindingproteincontainingDNA-binding,oligomerizationandtranscriptionactivationdomains.Itispostulatedtobindasatetramertoap53-bindingsiteandactivateexpressionofdownstreamgenesthatinhibitgrowthand/orinvasion,andthusfunctionasatumorsuppressor.Mutantsofp53thatfrequentlyoccurinanumberofdifferenthumancancersfailtobindtheconsensusDNAbindingsite,andhencecausethelossoftumorsuppressoractivity.AlterationsoftheTP53geneoccurnotonlyassomaticmutationsinhumanmalignancies,butalsoasgermlinemutationsinsomecancer-pronefamilieswithLi-Fraumenisyndrome. |
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| UniProtSummary | FUNCTION:SwissProt:P04637#Actsasatumorsuppressorinmanytumortypes;inducesgrowtharrestorapoptosisdependingonthephysiologicalcircumstancesandcelltype.Involvedincellcycleregulationasatrans-activatorthatactstonegativelyregulatecelldivisionbycontrollingasetofgenesrequiredforthisprocess.Oneoftheactivatedgenesisaninhibitorofcyclin-dependentkinases.ApoptosisinductionseemstobemediatedeitherbystimulationofBAXandFASantigenexpression,orbyrepressionofBcl-2expression. COFACTOR:Binds1zincionpersubunit. SIZE:393aminoacids;43653Da SUBUNIT:InteractswithAXIN1.ProbablypartofacomplexconsistingofTP53,HIPK2andAXIN1(Bysimilarity).BindsDNAasahomotetramer.InteractswithhistoneacetyltransferasesEP300andmethyltransferasesHRMT1L2andCARM1,andrecruitsthemtopromoters.Invitro,theinteractionofTP53withcancer-associated/HPV(E6)viralproteinsleadstoubiquitinationanddegradationofTP53givingapossiblemodelforcellgrowthregulation.Thiscomplexformationrequiresanadditionalfactor,E6-AP,whichstablyassociateswithTP53inthepresenceofE6.C-terminusinteractswithTAF1,whenTAF1ispartoftheTFIIDcomplex.InteractswithING4andthisinteractionmaybeindirect.FoundinacomplexwithCABLES1andTP73.InteractswithHIPK1,HIPK2,andP53DINP1.InteractswithWWOX.MayinteractswithHCVcoreprotein.InteractswithUSP7andSYVN1.InteractswithHSP90AB1(Bysimilarity).InteractswithBANP. SUBCELLULARLOCATION:Cytoplasm.Nucleus.Endoplasmicreticulum.Note=InteractionwithBANPpromotesnuclearlocalization. DOMAIN:SwissProt:P04637Thenuclearexportsignalactsasatranscriptionalrepressiondomain. PTM:Acetylated.AcetylationofLys-382byCREBBPenhancestranscriptionalactivity.DeacetylationofLys-382bySIRT1impairsitsabilitytoinduceproapoptoticprogramandmodulatecellsenescence.&PhosphorylationonSerresiduesmediatestranscriptionalactivation.PhosphorylatedbyHIPK1(Bysimilarity).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. DISEASE:SwissProt:P04637#TP53isfoundinincreasedamountsinawidevarietyoftransformedcells.TP53isfrequentlymutatedorinactivatedinabout60%ofcancers.&DefectsinTP53areinvolvedinesophagealsquamouscellcarcinoma(ESCC)[MIM:133239].ESCCisatumoroftheesophagus.&DefectsinTP53areacauseofLi-Fraumenisyndrome(LFS)[MIM:151623].LFSisanautosomaldominantfamilialcancersyndromethatinitsclassicformisdefinedbytheexistenceofbothaprobandwithasarcomaandtwootherfirst-degreerelativeswithacancerbyage45years.Inthesefamiliestheaffectedrelativesdevelopadiversesetofmalignanciesatunusuallyearlyages.ThespectrumofcancersinLFSincludesbreastcarcinomas,soft-tissuesarcomas,braintumors,osteosarcoma,leukemiaandadreno-corticalcarcinoma.OtherpossiblecomponenttumorsofLFSaremelanoma,gonadalcelltumorsandcarcinomasofthelung,pancreasandprostate.&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]. SIMILARITY:Belongstothep53family. |
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品牌介绍
密理博(Millipore)公司成立于1954年，总部位于美国麻省，在全世界设有47个办事处，为100多个国家提供产品和技术服务。目前全球雇员超过5800人，在美国、法国和日本等国家拥有7家大型生产工厂，主要生产过滤膜及膜过滤产品。20世纪80年代，密理博公司进入中国市场。先后在香港、北京、上海、广州及成都设立了办事机构，并于2000年4月在上海浦东外高桥保税区建立了密理博（上海）贸易有限公司。为了更好地满足中国用户的需求，密理博中国主页于2006年11月向广大用户开放，介绍密理博中国有限公司的最新动态，力求为用户打造专业的产品与服务信息交流平台。
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