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ReliaTech/Rat AntiMouse MCSF R/103M37/100 µg188bio精品生物—专注于实验室精品爆款的电商平台 - 蚂蚁淘旗下精选188款生物医学科研用品
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ReliaTech/Rat AntiMouse MCSF R/103M37/100 µg

Clone/ABfeature:

(#7M23)

Antibodygeneration:

Thisantibodywasproducedfromahybridoma(mousemyelomafusedwithspleencellsfromamouse)immunizedwithhumanrecombinantproteinofM-CSFRextracellulardomain.

Antigen:

recombinantmouseM-CSFRECdoamin

Stability:

Lyophilizedsamplesarestablefor2yearsfromdateofreceiptwhenstoredat-70°C.Reconstitutedantibodycanbealiquotedandstoredfrozenat< -20 °C for at least for six months without detectable loss of activity.

Reconstitution:

Reconstitutetheantibodywith500µlsterilePBSandthefinalconcentrationis200µg/ml.

Description:

M-CSFreceptor,theproductofthec-fmsprotooncogene,isamemberofthetypeIIIsubfamilyofreceptortyrosinekinasesthatalsoincludesreceptorsforSCFandPDGF.Thesereceptorseachcontainfiveimmunoglobulinlikedomainsintheirextracellulardomain(ECD)andasplitkinasedomainintheirintracellularregion.M-CSFreceptorisexpressedprimarilyoncellsofthemonocyte/macrophagelineage,dendriticcells,stemcellsandinthedevelopingplacenta.HumanM-CSFreceptorcDNAencodesa972aminoacid(aa)typeImembraneproteinwitha19aasignalpeptide,a493aaextracellularregioncontainingtheligandbindingdomain,a25aatransmembranedomain,anda435aacytoplasmicdomain.ThehumanMCSFRECDshares60%,64%,72%,75%,75%,and76%aaidentitywithmouse,rat,bovine,canine,feline,andequineM-CSFR,respectively.ActivatorsofproteinkinaseCinduceTACE/ADAM17cleavageoftheMCSFreceptor,releasingthefunctionalligandbindingextracellulardomain.M-CSFbindinginducesreceptorhomodimerization,resultingintransphosphorylationofspecificcytoplasmictyrosineresiduesandsignaltransduction.TheintracellulardomainofactivatedMCSFRbindsmorethan150proteinsthataffectcellproliferation,survival,differentiationandcytoskeletalreorganization.Amongthese,PI3-Kinase,P42/44ERK,andcCblarekeytransducersofM-CSF-Rsignals.M-CSFRengagementiscontinuouslyrequiredformacrophagesurvivalandregulateslineagedecisionsandmaturationofmonocytes,macrophages,osteoclasts,andDC.M-CSF-Randintegrinαvβ3sharesignalingpathwaysduringosteoclastogenesisanddeletionofeithercausesosteopetrosis.Inthebrain,microgliaexpressingincreasedM-CSF-RareconcentratedwithAlzheimersaβpeptide,buttheirroleinpathogenesisisunclear.

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