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Millipore/05-1072 | Anti-Ras Antibody, (K-, H-, N-), clone 9A11.2/05-1072/100 µg
  • Millipore/05-1072 | Anti-Ras Antibody, (K-, H-, N-), clone 9A11.2/05-1072/100 µg

Millipore/05-1072 | Anti-Ras Antibody, (K-, H-, N-), clone 9A11.2/05-1072/100 µg

價格: ￥4932.00 市場價: 8220.00
貨號: 05-1072
品牌: Millipore
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    • Description
      CatalogueNumber05-1072
      BrandFamilyUpstate
      TradeName
      • Upstate
      DescriptionAnti-RasAntibody,(K-,H-,N-),clone9A11.2
      BackgroundInformationRas,aproto-oncogene,isasmallG-proteinthathas3primaryisoforms(H-Ras,N-Ras,andK-Ras)thatdifferinthereapproximately20C-terminalaminoacids.H-RaswasfirstdiscoveredasatransformingproducttheretrovirusHarveymurinevirusandK-RasofKirtensarcomavirus.Rasisaheavilystudiedtargetofbothacademicandpharmaceuticalresearchbecauseofitsimplicationsinvariouspathwaysanddiseasesaswellasbeingmutatedinalargenumberofhumancancers.RasismostnotablytheactivatoroftheErk/MAPKkinasepathwayasactivatorofRaf,aswellasanactivatorofPI3Kinase(PI3K).Initsoncogenic,mutatedstate,RasisunabletohydrolyzeGTPtoGDP,thusstayinginanactivestateandactivatingnumerouspathwaysincludingtheMAPKpathwaythroughitsactivationofRaf,butalsoothersaswellthatincludePI3KinaseandRalGDS.OnepaththatthepharmaceuticalindustryhastakentocontrolRasanditsactivityisbyfindingwhatsomeconsideritsAchilles’heel.Foritsactivation,Rasmustlocalizetotheplasmamembrane,butinterestingly,itlacksatransmembranedomain.Toachievethis,Rasmustfirstundergoapost-translationalmodification(PTM)knownasprenylationorgeranylationatitsC-terminalCAAXmotif.Forthistotakeplace,acontrolledthreestepprocessmustoccur.ThefirststepintheprocessistheprenylationorgeranylationoftheCintheCAAXmotifthatisinitiatedbythecovalentattachmentoffarnesylgroupstothecysteinethatiscatalyzedbytheheterodimerenzymesfarnesyltransferases??and?.Afterthismodification,the–aaXofthemotifisproteolyticallyremovedviaRce1(RasConvertingEnzyme1),amembraneassociatedendoprotease,byamechanismthatisstillnotfullyunderstood.Finally,theC-terminalprenylcysteineisnowmethlylatedbyICMT(IsoprenylcysteineCarboxymethylTransferase).ThesedrugshaveyettopassclinicaltrialsthoughandthereisdoubtthattheywilleverbesuccessfulintreatingtumorsassociatedwithRasactivation.
      ProductInformation
      FormatPurified
      PresentationProteinGpurifiedmousemonoclonalinstoragebuffercontaining0.1MTris-Glycine(pH7.4),15mMNaCl,and0.05%NaN3.
      StorageandShippingInformation
      StorageConditionsStablefor1yearat4°Cfromdateofreceipt.
      HandlingRecommendations:Uponreceipt,andpriortoremovingthecap,centrifugethevialandgentlymixthesolution.
      Applications
      ApplicationThisAnti-RasAntibody,(K-,H-,N-),clone9A11.2isvalidatedforuseinWB,IH(P)forthedetectionofRas.
      KeyApplications
      • WesternBlotting
      • Immunohistochemistry(Paraffin)
      BIOLOGicalInformation
      ImmunogenFulllengthrecombinantGST-taggedhumanH-Ras.
      Clone9A11.2
      ConcentrationPleaserefertotheCertificateofAnalysisforthelot-specificconcentration.
      HostMouse
      SpecificityRecognizesK-,H-,andN-Ras(all3isofroms).
      IsotypeIgG1κ
      SpeciesReactivity
      • Human
      • Mouse
      • Rat
      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.
      MolecularWeight21kDa
      PhysicochemicalInformation
      Dimensions
      MaterialsInformation
      MaterialsInformation
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