根据表面等离子体共振，9E9与FcγRIV具有强反应性，与FcγRII和FcγRIII的结合水平较低。在体内，仅当9E9首先结合同一效应细胞上的FcγRIV时，9E9才结合并阻断FcγRIII，导致同时抑制FcγRIII和FcγRIV。天然9E9通过Fc与FcγRII和FcγRIII结合。9000000000的阻断研究表明，FcγRIV是体内IgG2a和IgG2b介导的血小板清除所必需的。此外，用9E9阻断FcγRIV可减少B细胞耗竭。9E9还干扰免疫复合物与FcγRIV的结合，并可阻断巨噬细胞和中性粒细胞上的FcγRIII。 抗小鼠CD16.2（9 E9）体内抗体-低内毒素该产品同种型对照：Armenian Hamster IgG Isotype Control for In Vivo - Low Endotoxin [PIP] (ICH2251) 缓冲液：ICH3001-100ml，nICH3002-100ml，nICH3003-100ml， 浓度：≥ 2.0 mg/ml 纯度：>95% by SDS-PAGE 内毒素：<1.0 EU/mg as determined by the LAL method 制剂：Sterile, preservative-free, solution in PBS. BSA and Azide free.
应用类型
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.
