4000-520-616
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4000-520-616
当前位置: 首页 > 产品中心 > Other_recombinant_protein > Prosci/BID重组蛋白/91-089/0.05毫克
商品详细Prosci/BID重组蛋白/91-089/0.05毫克
Prosci/BID重组蛋白/91-089/0.05毫克
Prosci/BID重组蛋白/91-089/0.05毫克
商品编号: 91-089
品牌: prosci-inc
市场价: ¥7500.00
美元价: 4500.00
产地: 美国(厂家直采)
公司:
产品分类: 其它重组蛋白
公司分类: Other_recombinant_protein
联系Q Q: 3392242852
电话号码: 4000-520-616
电子邮箱: info@ebiomall.com
商品介绍

Specifications

SPECIES:Human
SOURCESPECIES:E.coli
SEQUENCE:Met1-Asp195
FUSIONTAG:TagFree
TESTEDAPPLICATIONS:
APPLICATIONS:ThisrecombinantproteincanbeusedforBIOLOGicalassays.Forresearchuseonly.

Properties

PURITY:Greaterthan95%asdeterminedbyreducingSDS-PAGE.
Endotoxinlevellessthan0.1ng/ug(1IEU/ug)asdeterminedbyLALtest.
PREDICTEDMOLECULARWEIGHT:21.99kD
PHYSICALSTATE:Liquid
BUFFER:Suppliedasa0.2umfilteredsolutionof20mMPB,100mMKCl,pH7.4.Itisnotrecommendedtoreconstitutetoaconcentrationlessthan100ug/ml.DissolvethelyophilizedproteininddH2O.
STORAGECONDITIONS:Storeat-20˚C,stablefor6monthsafterreceipt.
Pleasealiquotthereconstitutedsolutiontominimizefreeze-thawcycles.

AdditionalInfo

ALTERNATENAMES:BH3-InteractingDomainDeathAgoNIST,p22BID,BID
ACCESSIONNO.:P55957

Background

BH3-InteractingDomainDeathAgonist(BID)isamemberoftheBcl-2proteinfamilywhichregulatesoutermitochondrialmembranepermeABIlity.BIDisapro-apoptoticmemberthatcausescytochromectobereleasedfromthemitochondriaintermembranespaceintothecytosol.InteractionofBidwithBakcausesalteredmitochondrialmembranepermeability.BIDcontainsonlytheBH3domain,whichisrequiredforitsinteractionwiththeBcl-2familyproteinsandforitspro-deathactivity.BIDissusceptIBLetoproteolyticcleavagebycaspases,calpains,GranzymeBandcathepsins.Itisanintegratingkeyregulatoroftheintrinsicdeathpathwaythatamplifiescaspase-dependentandcaspase-independentexecutionofneuronalapoptosis.ThereforepharmacologicalinhibitionofBIDprovidesapromisingtherapeuticstrategyinneurologicaldiseaseswhereprogrammedcelldeathisprominent,andalsoofferanewstrategyforthetreatmentofacuterenalfailureassociatedwithischemia-reperfusion.BIDreceivesdirectinputsfromakeyregulatorofthecellcyclearrest/DNArepairmachinery(ATM),andthereforeisanexcellentcandidatetocoordinategenotoxicstressresponsesandapoptoticcelldeath.BIDisanovelpro-apoptosisBcl-2familyproteinthatisactivatedbycaspase8inresponsetoFas/TNF-R1deathreceptorsignals.DeletionofBIDinhibitscarcinogenesisintheliver,althoughthisgeneticalterationpromotestumOrigenesisinthemyeloidcells.ThisislikelyrelatedtothefunctionofBIDtopromotecellcycleprogressionintoSphase.BIDcouldbealsoinvolvedinthemaintenanceofgenomicstabilitybyengagingatmitosischeckpoint.
品牌介绍
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