根據(jù)表面等離子體共振,9E9與FcγRIV具有強(qiáng)反應(yīng)性,與FcγRII和FcγRIII的結(jié)合水平較低。在體內(nèi),僅當(dāng)9E9首先結(jié)合同一效應(yīng)細(xì)胞上的FcγRIV時(shí),9E9才結(jié)合并阻斷FcγRIII,導(dǎo)致同時(shí)抑制FcγRIII和FcγRIV。天然9E9通過Fc與FcγRII和FcγRIII結(jié)合。9000000000的阻斷研究表明,F(xiàn)cγRIV是體內(nèi)IgG2a和IgG2b介導(dǎo)的血小板清除所必需的。此外,用9E9阻斷FcγRIV可減少B細(xì)胞耗竭。9E9還干擾免疫復(fù)合物與FcγRIV的結(jié)合,并可阻斷巨噬細(xì)胞和中性粒細(xì)胞上的FcγRIII。 抗小鼠CD16.2(9 E9)體內(nèi)抗體-超低內(nèi)毒素該產(chǎn)品同種型對(duì)照:Armenian Hamster IgG Isotype Control for In Vivo - Low Endotoxin [PIP] (ICH2251) 緩沖液:ICH3001-100ml,nICH3002-100ml,nICH3003-100ml, 濃度:≥ 2.0 mg/ml 純度:>98% by SDS-PAGE and HPLC 內(nèi)毒素:≤ 0.5 EU/mg as determined by the LAL method 制劑:Sterile, preservative-free, solution in PBS. BSA and Azide free.
應(yīng)用類型
Blocking, Flow Cytometry
免疫原
9E9 was produced by immunizing Armenian hamsters with an FcγRIV-IgG1 fusion protein consisting of the extracellular domain of FcγRIV fused to a mouse IgG1 Fc portion (D265A-variant deficient in Fc-receptor binding). Splenic B cells were then fused to a mouse fusion partner, and hybridoma clones were screened for binding to CHO-K1-FcγRIV cells expressing FcγRIV.