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Millipore/FCMAB148F | Anti-Ras -FITC Antibody, clone RAS10/FCMAB148F/100 tests
  • Millipore/FCMAB148F | Anti-Ras -FITC Antibody, clone RAS10/FCMAB148F/100 tests

Millipore/FCMAB148F | Anti-Ras -FITC Antibody, clone RAS10/FCMAB148F/100 tests

價(jià)格: ￥3204.00 市場(chǎng)價(jià): 5340.00
貨號(hào): FCMAB148F
品牌: Millipore
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    • Description
      CatalogueNumberFCMAB148F
      DescriptionAnti-Ras-FITCAntibody,cloneRAS10
      AlternateNames
      • GTP-andGDP-bindingpeptideB
        GTPaseHras
        Ha-Ras1proto-oncoprotein
        RasfamilysmallGTPbindingproteinH-Ras
        Transformingproteinp2
        c-has/basp21protein
        c-ras-Ki-2activatedoncogene
        p19H-RasIDXprotein
        transformationgene:oncogeneHAMSV
        v-Ha-rasHarveyratsarcomaviraloncogenehomolog
      BackgroundInformationThetumoroncoproteinsHRas,KRas,andNRasareratedasRasprotoncogenes.PointmutationswithinRasgenesarefrequentlydetectedinhumanmalignanciesandinexperimentallyinducedtumorsinanimals.
      ProductInformation
      FormatFITC
      Control
      • MCF-7cells.
      PresentationPurifiedmousemonoclonalIgG2aκconjugatedtoFITCinPBSwith0.1%sodiumazideand15mg/mLBSA.
      StorageandShippingInformation
      StorageConditionsMaintainrefrigeratedat2-8°Cprotectedfromlightinundilutedaliquotsforupto6monthsfromdateofreceipt.
      Applications
      ApplicationAnti-Ras-FITCAntibody,cloneRAS10isanantibodyagainstRasforuseinFC.
      KeyApplications
      • FlowCytometry
      BIOLOGicalInformation
      ImmunogenPurifiedrecombinantRas.
      CloneRAS10
      ConcentrationPleaserefertotheCertificateofAnalysisforthelot-specificconcentration.
      HostMouse
      SpecificityThisantibodyrecognizesp21H-,K-andN-Ras.
      IsotypeIgG2a
      SpeciesReactivity
      • Human
      SpeciesReactivityNoteTestedandpassedonHuman.Unconjugatedantibody(05-519)isknowntoreacttoRatandMouse.
      AntibodyTypeMonoclonalAntibody
      EntrezGeneNumber
      EntrezGeneSummaryMembersoftheRASsuperfamilyofGTP-bindingproteins,whichincludesMRAS,aremembrane-anchored,intracellularsignaltransducersresponsIBLeforavarietyofnormalcellularfunctions.Theyareoncogenicallyactivatedinasignificantfractionoftumors.[suppliedbyOMIM]
      GeneSymbol
      • K-Ras
      • Ki-Ras
      • K-Ras2
      • Kras-2
      • p21B
      • KRAS
      • RASK2
      • HRAS
      • HA_RAS
      • N-RAS
      • H-RAS
      • NRAS
      • NRAS1
      • ALPS4
      PurificationMethodProteinGPurified
      UniProtNumber
      UniProtSummaryFUNCTION:RasproteinsbindGDP/GTPandpossessintrinsicGTPaseactivity.

      Enzymeregulation:AlternatebetweenaninactiveformboundtoGDPandanactiveformboundtoGTP.Activatedbyaguaninenucleotide-exchangefactor(GEF)andinactivatedbyaGTPase-activatingprotein(GAP).

      SIZE:189aminoacids;21,656Da

      SUBUNIT:InteractswithPHLPP(Bysimilarity).

      SUBCELLULARLOCATION:Cellmembrane;Lipid-anchor;Cytoplasmicside.

      Involvementindisease:

      DefectsinKRASareacauseofacutemyelogenousleukemia(AML)[MIM:601626].AMLisamalignantdiseaseinwhichhematopoieticprecursorsarearrestedinanearlystageofdevelopment.


      DefectsinKRASareacauseofjuvenilemyelomonocyticleukemia(JMML)[MIM:607785].JMMLisapediatricmyelodysplasticsyndromethatconstitutesapproximately30%ofchildhoodcasesofmyelodysplasticsyndrome(MDS)and2%ofleukemia.ItischaracterizedbyleukocytosiswithtissueinfiltrationandinvitrohypersensitivityofmyeloidProgenitorstogranulocyte-macrophagecolonystimulatingfactor.


      DefectsinKRASarethecauseofNoonansyndrome3(NS3)[MIM:609942].Noonansyndrome(NS)[MIM:163950]isadisordercharacterizedbydysmorphicfacialfeatures,shortstature,hypertelorism,cardiacanomalies,deafness,motordelay,andableedingdiathesis.Itisageneticallyheterogeneousandrelativelycommonsyndrome,withanestimatedincidenceof1in1000-2500livebirths.Rarely,NSisassociatedwithjuvenilemyelomonocyticleukemia(JMML).NS3inheritanceisautosomaldominant.


      DefectsinKRASareacauseofcardiofaciocutaneoussyndrome(CFCsyndrome)[MIM:115150];alsoknownascardio-facio-cutaneoussyndrome.CFCsyndromeischaracterizedbyadistinctivefacialappearance,heartdefectsandmentalretardation.Heartdefectsincludepulmonicstenosis,atrialseptaldefectsandhypertrophiccardiomyopathy.Someaffectedindividualspresentwithectodermalabnormalitiessuchassparse,friablehair,hyperkeratoticskinlesionsandageneralizedichthyosis-likecondition.TypicalfacialfeaturesaresimilartoNoonansyndrome.Theyincludehighforeheadwithbitemporalconstriction,hypoplasticsupraorbitalridges,downslantingpalpebralfissures,adepressednasalbridge,andposteriorlyangulatedearswithprominenthelices.TheinheritanceofCFCsyndromeisautosomaldominant.


      KRASmutationsareinvolvedincancerdevelopment
      MolecularWeight~21kDaCalculated
      PhysicochemicalInformation
      Dimensions
      MaterialsInformation
      MaterialsInformation
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