根據表面等離子體共振，9E9與FcγRIV具有強反應性，與FcγRII和FcγRIII的結合水平較低。在體內，僅當9E9首先結合同一效應細胞上的FcγRIV時，9E9才結合并阻斷FcγRIII，導致同時抑制FcγRIII和FcγRIV。天然9E9通過Fc與FcγRII和FcγRIII結合。9000000000的阻斷研究表明，FcγRIV是體內IgG2a和IgG2b介導的血小板清除所必需的。此外，用9E9阻斷FcγRIV可減少B細胞耗竭。9E9還干擾免疫復合物與FcγRIV的結合，并可阻斷巨噬細胞和中性粒細胞上的FcγRIII。 抗小鼠CD16.2（9 E9）體內抗體-超低內毒素該產品同種型對照：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.
