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Millipore/AB9927 | Anti-phospho-Akt1 (Tyr326) Antibody/AB9927/100 µg
Millipore/AB9927 | Anti-phospho-Akt1 (Tyr326) Antibody/AB9927/100 µg
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产品分类:
功能性抗体
公司分类:
Functional_antibody
联系Q Q:
3392242852
电话号码:
4000-520-616
电子邮箱:
info@ebiomall.com
商品介绍
Description | |
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CatalogueNumber | AB9927 |
Replaces | 09-288 |
Description | Anti-phospho-Akt1(Tyr326)Antibody |
AlternateNames |
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BackgroundInformation | Theserine/threoninekinaseAktfamilycontainsseveralmembers,includingAkt1(alsodesignatedPKBorRacPK),Akt2(alsodesignatedPKB-βorRacPK-β)andAkt3(alsodesignatedPKB-γorthyomaviralproto-oncogene3),whichexhibitsequencehomologywiththeproteinkinaseAandCfamiliesandareencodedbythec-Aktproto-oncogene.AllmembersoftheAktfamilyhaveaPleckstrinhomologydomain.Akt1andAkt2areactivatedbyPDGFstimulation.ThisactivationisdependentonPDGFR-βtyrosineresidues740and751,whichbindthe85kDasubunitofthephosphatidylinositol3-kinase(PI3-kinase)complex.TheactivationofAkt1andAkt2isinhibitedbythePIkinaseinhibitorwortmannin.Takentogether,thisdatastronglysuggeststhattheproteinsignalsdownstreamofthePIkinases. |
ProductInformation | |
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Format | AffinityPurified |
Control |
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Presentation | Purifiedrabbitpolyclonalinbuffercontaining0.1MTris-Glycine(pH7.4),150mMNaClwith0.05%sodiumazide. |
StorageandShippingInformation | |
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StorageConditions | Stablefor1yearat2-8°Cfromdateofreceipt. |
Applications | |
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Application | Detectphospho-Akt1(Tyr326)usingthisAnti-Akt1AntibodyvalidatedforuseinWB. |
KeyApplications |
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BIOLOGicalInformation | |
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Immunogen | KLH-conjugatedlinearpeptidecorrespondingtohumanAkt1phosphorylatedatTyr326. |
Epitope | PhosphorylatedTyr326 |
Concentration | PleaserefertotheCertificateofAnalysisforthelot-specificconcentration. |
Host | Rabbit |
Specificity | ThisantibodyrecognizesAkt1phosphorylatedatTyr326. |
SpeciesReactivity |
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SpeciesReactivityNote | DemonstratedtoreactwithHuman.PredictedtoreactwithMouse,Rat,Canine,andXenopusbasedon100%sequencehomology. |
AntibodyType | PolyclonalAntibody |
EntrezGeneNumber | |
EntrezGeneSummary | Theserine-threonineproteinkinaseencodedbytheAKT1geneiscatalyticallyinactiveinserum-starvedprimaryandimmortalizedfibroblasts.AKT1andtherelatedAKT2areactivatedbyplatelet-derivedgrowthfactor.Theactivationisrapidandspecific,anditisabrogatedbymutationsinthepleckstrinhomologydomainofAKT1.Itwasshownthattheactivationoccursthroughphosphatidylinositol3-kinase.InthedevelopingnervoussystemAKTisacriticalmediatorofgrowthfactor-inducedneuronalsurvival.Survivalfactorscansuppressapoptosisinatranscription-independentmannerbyactivatingtheserine/threoninekinaseAKT1,whichthenphosphorylatesandinactivatescomponentsoftheapoptoticmachinery.Multiplealternativelysplicedtranscriptvariantshavebeenfoundforthisgene.[providedbyRefSeq]. |
GeneSymbol |
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Modifications |
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PurificationMethod | AffinityPurfied |
UniProtNumber | |
UniProtSummary | FUNCTION:PlaysaroleasakeymodulatoroftheAKT-mTORsignalingpathwaycontrollingthetempooftheprocessofnewbornneuronsintegrationduringadultneurogenesis,includingcorrectneuronpositioning,dendriticdevelopmentandsynapseformation(Bysimilarity).Generalproteinkinasecapableofphosphorylatingseveralknownproteins.PhosphorylatesTBC1D4.Signalsdownstreamofphosphatidylinositol3-kinase(PI3K)tomediatetheeffectsofvariousgrowthfactorssuchasplatelet-derivedgrowthfactor(PDGF),epidermalgrowthfactor(EGF),insulinandinsulin-likegrowthfactorI(IGF-I).Playsaroleinglucosetransportbymediatinginsulin-inducedtranslocationoftheGLUT4glucosetransportertothecellsurface.MediatestheantiapoptoticeffectsofIGF-I.Mediatesinsulin-stimulatedproteinsynthesisbyphosphorylatingTSC2at"Ser-939"and"Thr-1462",therebyactivatingmTORC1signalingandleADIngtobothphosphorylationof4E-BP1andinactivationofRPS6KB1.Promotesglycogensynthesisbymediatingtheinsulin-inducedactivationofglycogensynthase.TheactivatedformcansuppressFoxOgenetranscriptionandpromotecellcycleprogression.EssentialfortheSPATA13-mediatedregulationofcellmigrationandadhesionassemblyanddisassembly.Ref.6Ref.10Ref.14Ref.15Ref.17Ref.19CATALYTICACTIVITY:ATP+aprotein=ADP+aphosphoprotein. ENZYMEREGULATION:Threespecificsites,oneinthekinasedomain(Thr-308)andthetwootheronesintheC-terminalregulatoryregion(Ser-473andTyr-474),needtobephosphorylatedforitsfullactivation. SUBUNITSTRUCTURE:InteractswithAGAP2(isoform2,PIKE-A),theinteractionrequiresguaninenucleotidesandstimulatesthekinaseactivity.Interacts(viatheC-terminus)withCCDC88A(viaitsC-terminus)andTHEM4(viaitsC-terminus).InteractswithAKTIP.Interacts(viaPHdomain)withMTCP1,TCL1AANDTCL1B.InteractswithTRAF6.InteractswithGRB10;theinteractionleadstoGRB10phosphorylationthuspromotingYWHAEbinding.InteractswithRARA;theinteractionphosphorylatesRARAandrepressesitstransactivationactivity.InteractswithTNK2. SUBCELLULARLOCATION:Cytoplasm.Nucleus.Cellmembrane.Note:Nucleusafteractivationbyintegrin-linkedproteinkinase1(ILK1).NucleartranslocationisenhancedbyinteractionwithTCL1A.PhosphorylationonTyr-176byTNK2resultsinitslocalizationtothecellmembranewhereitistargetedforfurtherphosphorylationsonThr-308andSer-473leadingtoitsactivationandtheactivatedformtranslocatestothenucleus. TISSUESPECIFICTY:Expressedinallhumancelltypessofaranalyzed.TheTyr-176phosphorylatedformshowsasignificantincreaseinexpressioninbreastcancersduringtheprogressivestagesi.e.normaltohyperplasia(ADH),ductalcarcinomainsitu(DCIS),invasiveductalcarcinoma(IDC)andlymphnodemetastatic(LNMM)stages.DOMAIN:BindingofthePHdomaintothephosphatidylinositol3-kinasealpha(PI3K)resultsinitstargetingtotheplasmamembrane.ThePHdomainmediatesinteractionwithTNK2andTyr-176isalsoessentialforthisinteraction. TheAGC-kinaseC-terminalmediatesinteractionwithTHEM4. PTM:PhosphorylationonThr-308,Ser-473andTyr-474isrequiredforfullactivity.ActivatedTNK2phosphorylatesitonTyr-176resultinginitsbindingtotheanionicplasmamembranephospholipidPA.Thisphosphorylatedformlocalizestothecellmembrane,whereitistargetedbyPDPK1andPDPK2forfurtherphosphorylationsonThr-308andSer-473leadingtoitsactivation.Ser-473phosphorylationbymTORC2favorsThr-308phosphorylationbyPDPK1.Ser-473phosphorylationisenhancedbyinteractionwithAGAP2isoform2(PIKE-A).Ser-473phosphorylationisenhancedinfocalcorticaldysplasiaswithTaylor-typeballooncells. Ubiquitinated;undergoesboth"Lys-48"-and"Lys-63"-linkedpolyubiquitination.TRAF6-induced"Lys-63"-linkedAKT1ubiquitinationiscriticalforphosphorylationandactivation.Whenubiquitinated,ittranslocatestotheplasmamembrane,whereitbecomesphosphorylated.Whenfullyphosphorylatedandtranslocatedintothenucleus,undergoes"Lys-48"-polyubiquitinationcatalyzedbyTTC3,leadingtoitsdegradationbytheproteasome.Ref.10Ref.14Ref.17Ref.34Ref.8Ref.20Ref.9Ref.16Ref.21Ref.26Ref.27INVOLVEMENTINDISEASE:DefectsinAKT1areacauseofsusceptibilitytobreastcancer(BC)[MIM:114480].Acommonmalignancyoriginatingfrombreastepithelialtissue.Breastneoplasmscanbedistinguishedbytheirhistologicpattern.Invasiveductalcarcinomaisbyfarthemostcommontype.Breastcancerisetiologicallyandgeneticallyheterogeneous.Importantgeneticfactorshavebeenindicatedbyfamilialoccurrenceandbilateralinvolvement.Mutationsatmorethanonelocuscanbeinvolvedindifferentfamiliesoreveninthesamecase. DefectsinAKT1areassociatedwithcolorectalcancer(CRC)[MIM:114500]. DefectsinAKT1areassociatedwithsusceptibilitytoovariancancer[MIM:604370];alsocalledsusceptibilitytofamilialbreast-ovariancancertype1(BROVCA1). SEQUENCESIMILARITIES:Belongstotheproteinkinasesuperfamily.AGCSer/Thrproteinkinasefamily.RACsubfamily. Contains1AGC-kinaseC-terminaldomain. Contains1PHdomain. Contains1proteinkinasedomain. |
MolecularWeight | ~56kDaobserved |
PhysicochemicalInformation |
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Dimensions |
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MaterialsInformation |
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MaterialsInformation |
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品牌介绍
密理博(Millipore)公司成立于1954年,总部位于美国麻省,在全世界设有47个办事处,为100多个国家提供产品和技术服务。目前全球雇员超过5800人,在美国、法国和日本等国家拥有7家大型生产工厂,主要生产过滤膜及膜过滤产品。20世纪80年代,密理博公司进入中国市场。先后在香港、北京、上海、广州及成都设立了办事机构,并于2000年4月在上海浦东外高桥保税区建立了密理博(上海)贸易有限公司。为了更好地满足中国用户的需求,密理博中国主页于2006年11月向广大用户开放,介绍密理博中国有限公司的最新动态,力求为用户打造专业的产品与服务信息交流平台。
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