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Millipore/MABE171 |抗磷酸化组蛋白H2A.X（Thr120）抗体，克隆11F5.3/MABE171/100µ；G
Millipore/MABE171 |抗磷酸化组蛋白H2A.X（Thr120）抗体，克隆11F5.3/MABE171/100µ；G
市场价：
¥0.00
美元价：
0.00
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 | |
|---|---|
| CatalogueNumber | MABE171 |
| Description | Anti-phospho-HistoneH2A.X(Thr120)Antibody,clone11F5.3 |
| AlternateNames |
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| BackgroundInformation | HistoneH2A.XisavariantofhistoneH2A,andissimilarlyassociatedwithgenomicDNA.However,histoneisstructurallydifferentfromothermembersoftheH2AfamilyinpossessingaC-terminaltailthatcontainstheSer139residuethatisphosphorylatedinresponsetobreaksindouble-strandedDNA.ThephosphorylationofH2A.XisarapidprocessthatismediatedbyATM/ATRproteins. |
| ProductInformation | |
|---|---|
| Format | Purified |
| Control |
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| Presentation | PurifiedmousemonoclonalIgG3κinbuffercontaining0.1MTris-Glycine(pH7.4),150mMNaClwith0.05%sodiumazide. |
| StorageandShippingInformation | |
|---|---|
| StorageConditions | Stablefor1yearat2-8°Cfromdateofreceipt. |
| BIOLOGicalInformation | |
|---|---|
| Immunogen | KLH-conjugatedlinearpeptidecorrespondingtoHistoneH2A.XphosphorylatedatThr120. |
| Epitope | PhosphorylatedThr120 |
| Clone | 11F5.3 |
| Concentration | PleaserefertotheCertificateofAnalysisforthelot-specificconcentration. |
| Host | Mouse |
| Specificity | ThisantibodyrecognizesHistoneH2A.XphosphorylatedatThr120. |
| SpeciesReactivity |
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| AntibodyType | MonoclonalAntibody |
| EntrezGeneNumber | |
| EntrezGeneSummary | HistonesarebasicnuclearproteinsthatareresponsIBLeforthenucleosomestructureofthechromosomalfiberineukaryotes.Twomoleculesofeachofthefourcorehistones(H2A,H2B,H3,andH4)formanoctamer,aroundwhichapproximately146bpofDNAiswrappedinrepeatingunits,callednucleosomes.Thelinkerhistone,H1,interactswithlinkerDNAbetweennucleosomesandfunctionsinthecompactionofchromatinintohigherorderstructures.ThisgeneencodesamemberofthehistoneH2Afamily,andgeneratestwotranscriptsthroughtheuseoftheconservedstem-loopterminationmotif,andthepolyAadditionmotif. |
| GeneSymbol |
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| Modifications |
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| PurificationMethod | ProteinGPurified |
| UniProtNumber | |
| UniProtSummary | FUNCTION:VarianthistoneH2AwhichreplacesconventionalH2Ainasubsetofnucleosomes.NucleosomeswrapandcompactDNAintochromatin,limitingDNAaccessibilitytothecellularmachinerieswhichrequireDNAasatemplate.Histonestherebyplayacentralroleintranscriptionregulation,DNArepair,DNAreplicationandchromosomalstABIlity.DNAaccessibilityisregulatedviaacomplexsetofpost-translationalmodificationsofhistones,alsocalledhistonecode,andnucleosomeremodeling.Requiredforcheckpoint-mediatedarrestofcellcycleprogressioninresponsetolowdosesofionizingrADIationandforefficientrepairofDNAdoublestrandbreaks(DSBs)specificallywhenmodifiedbyC-terminalphosphorylation. SUBUNITSTRUCTURE:ThenucleosomeisahistoneoctamercontainingtwomoleculeseachofH2A,H2B,H3andH4assembledinoneH3-H4heterotetramerandtwoH2A-H2Bheterodimers.Theoctamerwrapsapproximately147bpofDNA.InteractswithnumerousproteinsrequiredforDNAdamagesignalingandrepairwhenphosphorylatedonSer-140.TheseincludeMDC1,TP53BP1,BRCA1andtheMRNcomplex,composedofMRE11A,RAD50,andNBN.InteractionwiththeMRNcomplexismediatedatleastinpartbyNBN.AlsointeractswithDHX9/NDHIIwhenphosphorylatedonSer-140.InteractswithARRB2;theinteractionisdetectedinthenucleusuponOR1D2stimulation. SUBCELLULARLOCATION:Nucleus.Chromosome. DEVELOPMENTSTAGE:SynthesizedinG1aswellasinS-phase. DOMAIN:The[ST]-QmotifconstitutesarecognitionsequenceforkinasesfromthePI3/PI4-kinasefamily. POST-TRANSLATIONALMODIFICATION:PhosphorylatedonSer-140(toformgamma-H2AFXorH2AX139ph)inresponsetoDNAdoublestrandbreaks(DSBs)generatedbyexogenousgenotoxicagentsandbystalledreplicationforks,andmayalsooccurduringmeioticrecombinationeventsandimmunoglobulinclassswitchinginlymphocytes.PhosphorylationcanextenduptoseveralthousandnucleosomesfromtheactualsiteoftheDSBandmaymarkthesurroundingchromatinforrecruitmentofproteinsrequiredforDNAdamagesignalingandrepair.Widespreadphosphorylationmayalsoservetoamplifythedamagesignaloraidrepairofpersistentlesions.PhosphorylationofSer-140(H2AX139ph)inresponsetoionizingradiationismediatedbybothATMandPRKDCwhiledefectsinDNAreplicationinduceSer-140phosphorylation(H2AX139ph)subsequenttoactivationofATRandPRKDC.DephosphorylationofSer-140byPP2AisrequiredforDNADSBrepair.Inmeiosis,Ser-140phosphorylation(H2AX139ph)mayoccuratsynaptonemalcomplexesduringleptoteneasanATM-dependentresponsetotheformationofprogrammedDSBsbySPO11.Ser-140phosphorylation(H2AX139ph)maysubsequentlyoccursatunsynapsedregionsofbothautosomesandtheXYbivalentduringzygotene,downstreamofATRandBRCA1activation.Ser-140phosphorylation(H2AX139ph)mayalsoberequiredfortranscriptionalrepressionofunsynapsedchromatinandmeioticsexchromosomeinactivation(MSCI),wherebytheXandYchromosomescondenseinpachytenetoformtheheterochromaticXY-body.Duringimmunoglobulinclassswitchrecombinationinlymphocytes,Ser-140phosphorylation(H2AX139ph)mayoccuratsitesofDNA-recombinationsubsequenttoactivationoftheactivation-inducedcytidinedeaminaseAICDA.PhosphorylationatTyr-143(H2AXY142ph)byBAZ1B/WSTFdeterminestherelativerecruitmentofeitherDNArepairorpro-apoptoticfactors.PhosphorylationatTyr-143(H2AXY142ph)favorstherecruitmentofAPBB1/FE65andpro-apoptosisfactorssuchasMAPK8/JNK1,triggeringapoptosis.Incontrast,dephosphorylationofTyr-143byEYAproteins(EYA1,EYA2,EYA3orEYA4)favorstherecruitmentofMDC1-containingDNArepaircomplexestothetailofphosphorylatedSer-140(H2AX139ph).MonoubiquitinationofLys-120(H2AXK119ub)byRING1andRNF2/RING2complexgivesaspecifictagforepigenetictranscriptionalrepression.FollowingDNAdouble-strandbreaks(DSBs),itisubiquitinatedthrough"Lys-63"linkageofubiquitinmoietiesbytheE2ligaseUBE2NandtheE3ligasesRNF8andRNF168,leadingtotherecruitmentofrepairproteinstositesofDNAdamage.Monoubiquitinationandionizingradiation-induced"Lys-63"-linkedubiquitinationaredistinctevents.AcetylationatLys-37increasesinSandG2phases.ThismodificationhasbeenproposedtoplayaroleinDNAdouble-strandbreakrepair. SEQUENCESIMILARITIES:BelongstothehistoneH2Afamily. |
| MolecularWeight | ~17kDaobserved |
| 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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