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            當前位置 : Millipore >>> 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

            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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