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Millipore/CBL404 | Anti-p53 Antibody, aa 211-220, clone240/CBL404/100 µg
Millipore/CBL404 | Anti-p53 Antibody, aa 211-220, clone240/CBL404/100 µg
市场价：
¥5340.00
美元价：
3204.00
产品分类：
功能性抗体
公司分类：
Functional_antibody
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 | CBL404 |
| Replaces | 04-1083 |
| BrandFamily | Chemicon® |
| TradeName |
|
| Description | Anti-p53Antibody,aa211-220,clone240 |
| BackgroundInformation | p53wasdiscoveredin1979asacellularproteinassociatingwiththetransformingproteinofSV40tumorvirus.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 | |
|---|---|
| Format | Purified |
| Presentation | Purifiedmousemonoclonalinbuffercontaining0.1MTris-glycine(pH7.4),0.15MNaCl,with0.05%sodiumazide.Werecommendthateachlaboratorydetermineanoptimumworkingtitreforuseinitsparticularapplication. |
| StorageandShippingInformation | |
|---|---|
| StorageConditions | Forusewithin1monthofpurchasestoreat+4°C,forlongtermstoragealiquotantibodyintosmallvolumesandstoreat-20°C. |
| BIOLOGicalInformation | |
|---|---|
| Immunogen | Murinep53-betagalactosidasefusionproteinexpressedinE.coli. |
| Epitope | aa211-220 |
| Clone | PAb240 |
| Host | Mouse |
| Specificity | PAb240recognizesanepitopeofp53tumorsuppressorproteinbetweenaminoacids211and220(Gannon,1990;Legros,1994)inhuman,mouse,rat,hamster,monkey,cowandchicken.Assayingnativesamples(immunoprecipitation,ELISA)thePAb240detectsonlythemutantformsofp53(Gannon,1990;Said,1994).Inmethodsusingdenaturedsamples[Westernblotanalysis(Gannon,1990)andimmunohistochemistryoffrozentissuesections(Said,1994;Bartek,1991;Walker,1991)],thePAb240recognizesbothmutantanddenaturedwild-typep53. |
| Isotype | IgG1 |
| SpeciesReactivity |
|
| AntibodyType | MonoclonalAntibody |
| 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. |
| GeneSymbol |
|
| UniProtNumber | |
| 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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