當(dāng)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(guī)格
數(shù)量
庫存(0)
特別 提示
代購產(chǎn)品:無質(zhì)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(lián)系客服核對商品價格,訂單生效后再付款。
資深產(chǎn)品顧問
咨詢顧問

全國免費服務(wù)熱線

4000-520-616


  • 自營商城 一站式服務(wù)
  • 廠家直采 剔除溢價
  • 品質(zhì)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(tài)度,由螞蟻淘公司專業(yè)人員負責(zé)品控、采購、物流、銷售、售后,保障正品優(yōu)質(zhì)。以“快速好省,為科研提供好產(chǎn)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(chǎn)品帶給科研!? 力求給你最優(yōu)質(zhì)的商品。
  • Q:生物188產(chǎn)品正品保障嗎?
    A:生物188質(zhì)量把控人員具有十年的從業(yè)經(jīng)驗,在業(yè)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(zé)國際物流和清關(guān),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(lián)系我們客服進行修改;客服電話:4000-520-616

    Q:可以開發(fā)票嗎?
    A:本網(wǎng)站所售商品都是正規(guī)清關(guān),均開具16%正規(guī)發(fā)票,發(fā)票金額含配送費金額,另有說明的除外。

    Q:商品幾天可以發(fā)貨?
    A:生物188商品,全部現(xiàn)貨銷售,付款后即可發(fā)貨,一般一周內(nèi)送達!

    Q:如何聯(lián)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(wù)熱線:4000-520-616 或聯(lián)系我們的在線客服QQ:1570468124

    Q:收到的商品少了/發(fā)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(fā)出,可能不會同時送達,建議查看訂單詳情是否是 部分發(fā)貨狀態(tài);如未收到,可聯(lián)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(chǎn)品一個月內(nèi)(以快遞公司顯示簽收時間為準(zhǔn)),包裝規(guī)格、 數(shù)量、品種不符,外觀毀損、短缺或缺陷,請在收到貨24小時內(nèi)申請退換貨;特殊商品以合同條款為準(zhǔn)。

何為188

極簡而嚴謹,我們僅銷售188款生物醫(yī)學(xué)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(chǎn)品,聚焦服務(wù)每一位客戶!

關(guān)注我們 :

點擊QQ聯(lián)系我們
生物188微信

關(guān)注188微信公眾號

獲取最新優(yōu)惠活動通知