首页|期刊导航|中华医学杂志（英文版）|Analysis of TRAIL receptor expression using anti-TRAIL death receptor-5 monoclonal antibodies
中华医学杂志（英文版）2003，Vol.116Issue(6)：947-950,4.
Analysis of TRAIL receptor expression using anti-TRAIL death receptor-5 monoclonal antibodies
Analysis of TRAIL receptor expression using anti-TRAIL death receptor-5 monoclonal antibodies
摘要
Abstract
ObjectiveTo establish hybridomas that produce anti-death receptor-5 (DR5) monoclonal antibodies (mAbs) and check the surface expression of DR5 (sDR5) on cell lines.MethodsThe cDNA of human DR5 was cloned into pGAPZα. Recombinant Pichia pastoris clones generated via homologous recombination secreted high levels of sDR5. The sDR5 was purified using a nickel ion column. BALB/c mice were immunized with sDR5 and spleen cells were fused with the SP2/0-Ag 14. Monoclonal antibodies were tested by ELISA for their abilities binding to sDR5 and by flow cytometry for thereactivities to surface DR5 of Jurkat cells. Surface expression of the TRAIL receptor was determined by flow cytometric analysis measuring the binding of anti-DR5 mAb. Resultse to sDR5 as observed through ELISA. It was discovered using flow cytometry that only IgG was able to bind to DR5 on the plasma membrane of Jurkat cells. sDR5was found to completely inhibit anti-DR5 mAb binding to Jurkat cells. Pproximately 95% of Jurkat cells, 98% SW480, 99% U937, 100% U87, 86% HCT116, 64% HL-60, 47% HeLa and 13% K562 cells express membrane DR5. ConclusionsThese results demonstrate that anti-DR5 mAb is able to specifically bind to DR5and that DR5 is expressed at high levels on Jurkat, SW480, U87, U937 and HCT116cell lines, and at medium levels on HL-60 and HeLa cell lines. The expressionof DR5 on K562 cell line is low.关键词
TRAIL/TRAIL-R/apoptosis/death receptor-5/monoclonal antibodyKey words
TRAIL/TRAIL-R/apoptosis/death receptor-5/monoclonal antibody分类
医药卫生引用本文复制引用
马远方,杨东亮,陈有海..Analysis of TRAIL receptor expression using anti-TRAIL death receptor-5 monoclonal antibodies[J].中华医学杂志（英文版）,2003,116(6):947-950,4.基金项目
This work was supported in part by grants HNIFOS 0321001800 and HNIFMSTS 2002-119. （）
