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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
市场价：
¥6160.00
美元价：
3696.00
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 | 06-1283 |
| Replaces | 06-915 |
| Description | Anti-acetyl-p53(Lys320)Antibody |
| AlternateNames |
|
| 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 | AffinityPurified |
| Control |
|
| Presentation | Purifiedrabbitpolyclonalinbuffercontaining0.1MTris-Glycine(pH7.4),150mMNaClwith0.05%sodiumazide. |
| StorageandShippingInformation | |
|---|---|
| StorageConditions | Stablefor1yearat2-8°Cfromdateofreceipt. |
| BIOLOGicalInformation | |
|---|---|
| Immunogen | KLH-conjugatedlinearpeptidecorrespondingtop53atLys320. |
| Epitope | AcetylLys320 |
| Concentration | PleaserefertotheCertificateofAnalysisforthelot-specificconcentration. |
| Host | Rabbit |
| Specificity | Thisantibodyrecognizesp53acetylatedatLys320. |
| SpeciesReactivity |
|
| SpeciesReactivityNote | Demonstratedtoreactwithhuman.Predictedtoreactwithchimpanzeeandbovinebasedon100%sequencehomology. |
| AntibodyType | PolyclonalAntibody |
| EntrezGeneNumber | |
| EntrezGeneSummary | Thisgeneencodestumorproteinp53,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 |
|
| PurificationMethod | AffinityPurfied |
| UniProtNumber | |
| UniProtSummary | FUNCTION: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 |
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| Dimensions |
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| MaterialsInformation |
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| MaterialsInformation |
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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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