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Millipore/04-775 | Anti-Ha-Ras Antibody, clone MC57, rabbit monoclonal/04-775/100 µL
  • Millipore/04-775 | Anti-Ha-Ras Antibody, clone MC57, rabbit monoclonal/04-775/100 µL

Millipore/04-775 | Anti-Ha-Ras Antibody, clone MC57, rabbit monoclonal/04-775/100 µL

價(jià)格: ￥3444.00 市場(chǎng)價(jià): 5740.00
貨號(hào): 04-775
品牌: Millipore
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    • Description
      CatalogueNumber04-775
      Replaces05-775
      DescriptionAnti-Ha-RasAntibody,cloneMC57,rabbitmonoclonal
      AlternateNames
      • GTP-andGDP-bindingpeptideB
      • GTPaseHRas
      • Ha-Ras1proto-oncoprotein
      • RasfamilysmallGTPbindingproteinH-Ras
      • Transformingproteinp21
      • c-has/basp21protein
      • c-ras-Ki-2activatedoncogene
      • p19H-RasIDXprotein
      • transformationgene:oncogeneHAMSV
      • v-Ha-rasHarveyratsarcomaviraloncogenehomolog
      BackgroundInformationRasproteinsaresmallGTP-bindingproteinswhich,unliketheheterotrimericG-proteins,containallGTPaseandeffectorfunctionswithinasinglepolypeptide.AtleastthreeisoformsofRasexist,Ki-Ras,Ha-RasandN-Ras,withdistinctexpressionpatternsbutsimilarsignalingactivity.Rasispalmitoylatedandfarnesylatedatthecarboxyterminus,anchoringitinthemembrane.Inrestingcells,RasisloadedwithGDP,andisactivatedsubsequenttogrowthfactorstimulationofreceptors,whichrecruitRasGuaninenucleotideExchangeFactorstotheplaneofthemembrane.ProximityofexchangefactorstotheRasproteinscausesreleaseofGDP,anditsreplacementbyGTP.InitsGTP-boundform,Rasbindsseveralproteins,includingRaf,RalGDSandPI3Kinase.InactivationofRasoccursbyGTPhydrolysis,whichisgreatlyacceleratedbyRasGAPorNF-1,twoknownRasGTPaseActivatingProteins.ItispossIBLetoassayforRasactivationbyincubationoflysateswiththeRas-bindingdomainofRaf-1,whichselectivelybindstoRas:GTP.
      ProductInformation
      FormatCultureSupernatant
      Control
      • IncludedPositiveAntigenControl:Catalog#12-301,non-stimulatedA431lysate.Add2.5μLof2-mercaptoethanol/100μLoflysateandboilfor5minutestoreducethepreparation.Load20μgofreducedlysateperlaneforminigels.
      PresentationCulturedsupernantantcontaining0.05%sodiumazide.
      StorageandShippingInformation
      StorageConditionsStablefor1yearat-20oCfromdateofreceipt.
      HandlingRecommendations:Uponreceipt,andpriortoremovingthecap,centrifugethevialandgentlymixthesolution.Aliquotintomicrocentrifugetubesandstoreat-20°C.Avoidrepeatedfreeze/thawcycles,whichmaydamageIgGandaffectproductperformance.
      Applications
      ApplicationDetectHa-RasusingthisAnti-Ha-RasAntibody,cloneMC57validatedforuseinWB.
      KeyApplications
      • WesternBlotting
      BIOLOGicalInformation
      ImmunogenGSTfusionproteincorrespondingtofulllengthhumanHa-Ras.CloneMC57.
      CloneMC57
      ConcentrationPleaserefertotheCertificateofAnalysisforthelot-specificconcentration.
      HostRabbit
      SpecificityRecognizesHa-Ras,Mr~21kDa.DoesnotcrossreactwithCdc42,RhoorRac1.
      IsotypeIgG
      SpeciesReactivity
      • Human
      • Mouse
      • Rat
      SpeciesReactivityNoteHuman.Predictedtocross-reactwithmouseandratbasedonsequencehomology.
      AntibodyTypeMonoclonalAntibody
      EntrezGeneNumber
      EntrezGeneSummaryThisgenebelongstotheRasoncogenefamily,whosemembersarerelatedtothetransforminggenesofmammaliansarcomaretroviruses.Theproductsencodedbythesegenesfunctioninsignaltransductionpathways.TheseproteinscanbindGTPandGDP,andtheyhaveintrinsicGTPaseactivity.Thisproteinundergoesacontinuouscycleofde-andre-palmitoylation,whichregulatesitsrapidexchangebetweentheplasmamembraneandtheGolgiapparatus.MutationsinthisgenecauseCostellosyndrome,adisease
      characterizedbyincreasedgrowthattheprenatalstage,growthdeficiencyatthepostnatalstage,predispositiontotumorformation,mentalretardation,skinandmusculoskeletalabnormalities,distinctivefacialappearanceandcardiovascularabnormalities.Defectsinthisgeneareimplicatedinavarietyofcancers,includingbladdercancer,follicularthyroidcancer,andoralsquamouscellcarcinoma.Multipletranscriptvariants,whichencodedifferentisoforms,havebeenidentifiedforthisgene.
      GeneSymbol
      • C-BAS/HAS
      • C-H-RAS
      • C-HA-RAS1
      • CTLO
      • H-RASIDX
      • H-Ras-1
      • HAMSV
      • HRAS1
      • Ha-Ras
      • K-RAS
      • N-RAS
      • OTTHUMP00000162769
      • OTTHUMP00000166053
      • OTTHUMP00000166055
      • RASH1
      • c-H-ras
      • p21ras
      UniProtNumber
      UniProtSummaryFUNCTION:RasproteinsbindGDP/GTPandpossessintrinsicGTPaseactivity.Ref.18Ref.32
      ENZYMEREGULATION:AlternatebetweenaninactiveformboundtoGDPandanactiveformboundtoGTP.Activatedbyaguaninenucleotide-exchangefactor(GEF)andinactivatedbyaGTPase-activatingprotein(GAP).
      SUBUNITSTRUCTURE:InitsGTP-boundforminteractswithPLCE1.InteractswithTBC1D10C.InteractswithRGL3Bysimilarity.FormsasignalingcomplexwithRASGRP1andDGKZ.InteractswithRASSF5.
      SUBCELLULARLOCATION:Cellmembrane;Lipid-anchor;Cytoplasmicside.Golgiapparatusmembrane;Lipid-anchor.Note:ShuttlesbetweentheplasmamembraneandtheGolgiapparatus.
      PTM:PalmitoylatedbytheZDHHC9-GOLGA7complex.Acontinuouscycleofde-andre-palmitoylationregulatesrapidexchangebetweenplasmamembraneandGolgi.S-nitrosylated;criticalforredoxregulation.Importantforstimulatingguaninenucleotideexchange.Nostructuralperturbationonnitrosylation.
      INVOLVEMENTINDISEASE:DefectsinHRASarethecauseofCostellosyndrome[MIM:218040];alsoknownasfaciocutaneoskeletalsyndrome.Costellosyndromeisarareconditioncharacterizedbyprenatallyincreasedgrowth,postnatalgrowthdeficiency,mentalretardation,distinctivefacialappearance,cardiovascularabnormalities(typicallypulmonicstenosis,hypertrophiccardiomyopathyand/oratrialtachycardia),tumorpredisposition,skinandmusculoskeletalabnormalities.
      DefectsinHRASarethecauseofcongenitalmyopathywithexcessofmusclespindles(CMEMS)[MIM:218040].CMEMSisavariantofCostellosyndrome.
      DefectsinHRASmaybeacauseofsusceptibilitytoHurthlecellthyroidcarcinoma[MIM:607464];alsoknownasHurthlecellthyroidneoplasia.Hurthlecellthyroidcarcinomaaccountsforapproximately3%ofallthyroidcancers.Althoughtheyareclassifiedasvariantsoffollicularneoplasms,theyaremoreoftenmultifocalandsomewhatmoreaggressiveandarelesslikelytotakeupiodinethanareotherfollicularneoplasms.Mutationswhichchangepositions12,13or61activatethepotentialofHRAStotransformculturedcellsandareimplicatedinavarietyofhumantumors.DefectsinHRASareacauseofbladdercancer.DefectsinHRASarethecauseoforalsquamouscellcarcinoma(OSCC).
      SEQUENCESIMILARITIES:BelongstothesmallGTPasesuperfamily.Rasfamily.
      MASSSPECTROMETRY:Molecularmassis6.223±2Dafrompositions112-166.DeterminedbyESI.Molecularmassis6.253±2Dafrompositions112-166.DeterminedbyESI.Includesonenitricoxidemolecule.
      MolecularWeight~21kDa
      PhysicochemicalInformation
      Dimensions
      MaterialsInformation
      MaterialsInformation
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