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Millipore/04-244 | Anti-phospho-p53 (Ser392) Antibody, clone EP155Y, rabbit monoclonal/04-244/100 µL
Millipore/04-244 | Anti-phospho-p53 (Ser392) Antibody, clone EP155Y, rabbit monoclonal/04-244/100 µL
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¥0.00
美元价：
0.00
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 | 04-244 |
| Description | Anti-phospho-p53(Ser392)Antibody,cloneEP155Y,rabbitmonoclonal |
| AlternateNames |
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| BackgroundInformation | Thep53geneismutatedinapproximatelyhalfofallhumancancers.Itisinvolvedinthecellularresponsetocytotoxicstresses,andtogetherwithp19ARF,inducesexpressionofp21Cip1,tocausecellcyclearrest.Inaddition,p53isabletoinduceapoptosis,bothbytranscriptionalandnon-transcriptionalmechanisms.Theamino-terminal83aminoacidsofp53containthetransactivationdomain,aswellastheregioninvolvedintranscription-independentgrowthsuppression.Thecarboxy-terminalregioncontainstheDNA-bindingdomain,whichisregulatedbythreephosphorylationevents,andpotentiallybyacetylationalso. |
| ProductInformation | |
|---|---|
| Format | Unpurified |
| Presentation | UnpurifiedrabbitmonoclonalIgGinbuffercontaining50mMTris-Glycine(pH7.4),0.15MNaCl,40%Glycerol,0.01%sodiumazideand0.05%BSA. |
| StorageandShippingInformation | |
|---|---|
| StorageConditions | Stablefor1yearat-20ºCfromdateofreceipt. HandlingRecommendations:Uponreceipt,andpriortoremovingthecap,centrifugethevialandgentlymixthesolution.Aliquotintomicrocentrifugetubesandstoreat-20°C.Avoidrepeatedfreeze/thawcycles,whichmaydamageIgGandaffectproductperformance.Note:VariABIlityinfreezertemperaturesbelow-20°Cmaycauseglycerolcontainingsolutionstobecomefrozenduringstorage. |
| BIOLOGicalInformation | |
|---|---|
| Immunogen | SyntheticpeptidecorrespondingtophosphorylatedSer392andsurroundingaminoacidsofhumanp53. |
| Epitope | PhosphorylatedSer392 |
| Clone | EP155Y |
| Host | Rabbit |
| Specificity | Thisantibodyrecognizesp53whenphosphorylatedonSer392. |
| Isotype | IgG |
| SpeciesReactivity |
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| SpeciesReactivityNote | ProventoreactwithHumanandRat. |
| AntibodyType | MonoclonalAntibody |
| 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 |
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| Modifications |
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| PurificationMethod | Unpurified |
| UniProtNumber | |
| UniProtSummary | FUNCTION:Actsasatumorsuppressorinmanytumortypes;inducesgrowtharrestorapoptosisdependingonthephysiologicalcircumstancesandcelltype.Involvedincellcycleregulationasatrans-activatorthatactstonegativelyregulatecelldivisionbycontrollingasetofgenesrequiredforthisprocess.Oneoftheactivatedgenesisaninhibitorofcyclin-dependentkinases.ApoptosisinductionseemstobemediatedeitherbystimulationofBAXandFASantigenexpression,orbyrepressionofBcl-2expression.Ref.48 CofactorBinds1zincionpersubunit. SUBUNITSTRUCTURE:InteractswithAXIN1.ProbablypartofacomplexconsistingofTP53,HIPK2andAXIN1Bysimilarity.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.InteractswithCHD8,leADIngtorecruithistoneH1andpreventtransactivationactivityBysimilarity.InteractswithARMC10,BANP,CDKN2AIPandE4F1. SUBCELLULARLOCATION:Cytoplasm.Nucleus.Endoplasmicreticulum.Note=InteractionwithBANPpromotesnuclearlocalization.Ref.51Ref.56 DOMAIN:Thenuclearexportsignalactsasatranscriptionalrepressiondomain.Ref.34 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.Ref.51Ref.24Ref.26Ref.31Ref.35Ref.36Ref.40Ref.41Ref.49Ref.53Ref.58Ref.59Ref.60 MaybeO-glycosylatedintheC-terminalbasicregion.StudiedinEB-1cellline.Ref.28 UbiquitinatedbySYVN1,whichleadstoproteasomaldegradation.Ref.56 MonomethylatedatLys-372bySETD7,leadingtostabilizeitandincreasetranscriptionalactivation.MonomethylatedatLys-370bySMYD2,leadingtodecreaseDNA-bindingactivityandsubsequenttranscriptionalregulationactivity.Lys-372monomethylationpreventstheinteractionwithSMYD2andsubsequenctmonomethylationatLys-370.Ref.50Ref.54Ref.55 DISEASE:TP53isfoundinincreasedamountsinawidevarietyoftransformedcells.TP53isfrequentlymutatedorinactivatedinabout60%ofcancers. DefectsinTP53areinvolvedinesophagealsquamouscellcarcinoma(ESCC)[MIM:133239].ESCCisatumoroftheesophagus. DefectsinTP53areacauseofLi-Fraumenisyndrome(LFS)[MIM:151623].LFSisanautosomaldominantfamilialcancersyndromethatinitsclassicformisdefinedbytheexistenceofaprobandaffectedbyasarcomabefore45yearswithafirstdegreerelativeaffectedbyanytumorbefore45yearsandanotherfirstdegreerelativewithanytumorbefore45yearsorasarcomaatanyage.OtherclinicaldefinitionsforLFShavebeenproposed(Ref.95andRef.98)andcalledLi-Fraumenilikesyndrome(LFL).Inthesefamiliesaffectedrelativesdevelopadiversesetofmalignanciesatunusuallyearlyages.Fourtypesofcancersaccountfor80%oftumorsoccurringinTP53germlinemutationcarriers:breastcancers,softtissueandbonesarcomas,braintumors(astrocytomas)andadrenocorticalcarcinomas.Lessfrequenttumorsincludechoroidplexuscarcinomaorpapillomabeforetheageof15,rhaBDomyosarcomabeforetheageof5,leukemia,Wilmstumor,malignantphyllodestumor,colorectalandgastriccancers.Ref.74Ref.75Ref.76Ref.77Ref.78Ref.97Ref.99Ref.104Ref.105 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.Ref.108 DefectsinTP53areacauseofoneformofhereditaryadrenocorticalcarcinoma(ADCC)[MIM:202300].ADCCisararechildhoodtumor,representingabout0.4%ofchildhoodtumors,withahighincidenceofassociatedtumors.ADCCoccurswithincreasedfrequencyinpatientswiththeBeckwith-Wiedemannsyndrome[MIM:130650]andisacomponenttumorinLi-Fraumenisyndrome[MIM:151623].Ref.107 SIMILARITY:Belongstothep53family. |
| MolecularWeight | 53kDa |
| PhysicochemicalInformation |
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| Dimensions |
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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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