• <menu id="uuusw"></menu>
  • <table id="uuusw"></table>
    當前位置 : Millipore >>> 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
    • 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

    價格: 試用 市場價: 0.00

    貨號: 04-244
    品牌: Millipore
    規格
    數量
    庫存(0)
    特別 提示
    代購產品:無質量問題不接受退換貨,下單前請仔細核對信息。
    下單后請及時聯系客服核對商品價格,訂單生效后再付款。
    資深產品顧問
    咨詢顧問

    全國免費服務熱線

    4000-520-616


    • 自營商城 一站式服務
    • 廠家直采 剔除溢價
    • 品質甄選 正品保證
    • 嚴控流程 只做188精品
    • 極速物流 如約送貨
    • 詳情
    • 使用說明
    • 常見問題
      • Description
        CatalogueNumber04-244
        DescriptionAnti-phospho-p53(Ser392)Antibody,cloneEP155Y,rabbitmonoclonal
        AlternateNames
        • AntigenNY-CO-13
        • Phosphoproteinp53
        • Tumorsuppressorp53
        • p53antigen
        • p53transformationsuppressor
        • p53tumorsuppressor
        • transformation-relatedprotein53
        • tumorproteinp53
        BackgroundInformationThep53geneismutatedinapproximatelyhalfofallhumancancers.Itisinvolvedinthecellularresponsetocytotoxicstresses,andtogetherwithp19ARF,inducesexpressionofp21Cip1,tocausecellcyclearrest.Inaddition,p53isabletoinduceapoptosis,bothbytranscriptionalandnon-transcriptionalmechanisms.Theamino-terminal83aminoacidsofp53containthetransactivationdomain,aswellastheregioninvolvedintranscription-independentgrowthsuppression.Thecarboxy-terminalregioncontainstheDNA-bindingdomain,whichisregulatedbythreephosphorylationevents,andpotentiallybyacetylationalso.
        ProductInformation
        FormatUnpurified
        PresentationUnpurifiedrabbitmonoclonalIgGinbuffercontaining50mMTris-Glycine(pH7.4),0.15MNaCl,40%Glycerol,0.01%sodiumazideand0.05%BSA.
        StorageandShippingInformation
        StorageConditionsStablefor1yearat-20oCfromdateofreceipt.
        HandlingRecommendations:Uponreceipt,andpriortoremovingthecap,centrifugethevialandgentlymixthesolution.Aliquotintomicrocentrifugetubesandstoreat-20°C.Avoidrepeatedfreeze/thawcycles,whichmaydamageIgGandaffectproductperformance.Note:VariABIlityinfreezertemperaturesbelow-20°Cmaycauseglycerolcontainingsolutionstobecomefrozenduringstorage.
        Applications
        ApplicationUseAnti-phospho-p53(Ser392)Antibody,cloneEP155Y(rabbitmonoclonalantibody)validatedinIHC(P),ICC,IP,WBtodetectphospho-p53(Ser392)alsoknownasAntigenNY-CO-13,Phosphoproteinp53,Tumorsuppressorp53,p53antigen.
        KeyApplications
        • Immunohistochemistry(Paraffin)
        • Immunocytochemistry
        • Immunoprecipitation
        • WesternBlotting
        ApplicationNotesImmunohistochemistry(Paraffin)Analysis:
        Anti-phospho-p53(Ser392)wasdilutedto1:200.


        ImmunofluorescentImmunocytochemistry:
        Cellswerestainedwithanti-phopsho-p53(Ser392)ata1:250dilution.

        Immunoprecipitation:
        A1:50dilutionofapreviouslotwasusedinIP.
        BIOLOGicalInformation
        ImmunogenSyntheticpeptidecorrespondingtophosphorylatedSer392andsurroundingaminoacidsofhumanp53.
        EpitopePhosphorylatedSer392
        CloneEP155Y
        HostRabbit
        SpecificityThisantibodyrecognizesp53whenphosphorylatedonSer392.
        IsotypeIgG
        SpeciesReactivity
        • Human
        • Rat
        SpeciesReactivityNoteProventoreactwithHumanandRat.
        AntibodyTypeMonoclonalAntibody
        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
        • FLJ92943
        • LFS1
        • P53
        • TRP53
        • p53
        Modifications
        • Phosphorylation
        PurificationMethodUnpurified
        UniProtNumber
        UniProtSummaryFUNCTION: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.

        MolecularWeight53kDa
        PhysicochemicalInformation
        Dimensions
        MaterialsInformation
        MaterialsInformation
      售后保障
      螞蟻淘生物188,秉承螞蟻淘一貫的嚴謹態度,由螞蟻淘公司專業人員負責品控、采購、物流、銷售、售后,保障正品優質。以“快速好省,為科研提供好產品、好價格”為理念,直接鏈接原廠家,從全國各地原制造商嚴格挑選188款科研精品,剔除品牌溢價,188生物新電商,把好的產品帶給科研!? 力求給你最優質的商品。
    • Q:生物188產品正品保障嗎?
      A:生物188質量把控人員具有十年的從業經驗,在業界享有良好的口碑;自營商城,直接從廠家采購, 自己的團隊負責國際物流和清關,中間沒有第三方,所有流程嚴格把控,100%保證正品,假一罰十。

      Q:下單后可以修改訂單嗎?
      A:下單后的商品付款之前可以修改;訂單付款成功,需要聯系我們客服進行修改;客服電話:4000-520-616

      Q:可以開發票嗎?
      A:本網站所售商品都是正規清關,均開具16%正規發票,發票金額含配送費金額,另有說明的除外。

      Q:商品幾天可以發貨?
      A:生物188商品,全部現貨銷售,付款后即可發貨,一般一周內送達!

      Q:如何聯系商家?
      A:有任何問題夠可以電話咨詢我們,全國24小時免費服務熱線:4000-520-616 或聯系我們的在線客服QQ:1570468124

      Q:收到的商品少了/發錯了怎么辦?
      A:同個訂單購買多個商品可能會分為一個以上包裹發出,可能不會同時送達,建議查看訂單詳情是否是 部分發貨狀態;如未收到,可聯系在線客服或者致電4000-520-616。

      Q:退換貨/維修需要多長時間?
      A:一般情況下,退貨處理周期為客戶收到產品一個月內(以快遞公司顯示簽收時間為準),包裝規格、 數量、品種不符,外觀毀損、短缺或缺陷,請在收到貨24小時內申請退換貨;特殊商品以合同條款為準。

    何為188

    極簡而嚴謹,我們僅銷售188款生物醫學科研用品,款款都是爆款;因為少所以聚焦,聚焦甄選每一款產品,聚焦服務每一位客戶!

    關注我們 :

    點擊QQ聯系我們
    生物188微信

    關注188微信公眾號

    獲取最新優惠活動通知
    • 品質甄選,正品保證

    • 自營電商,廠家直采

    • 極簡主義,188精品

  • <menu id="uuusw"></menu>
  • <table id="uuusw"></table>
    上床视频