作者: Isabel M. Olazabal , Emmanuelle Caron , Robin C. May , Kerstin Schilling , David A. Knecht
DOI: 10.1016/S0960-9822(02)01069-2
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摘要: Abstract Phagocytosis through Fcγ receptor (FcγR) or complement 3 (CR) requires Arp2/3 complex-mediated actin polymerization, although each uses a distinct signaling pathway [1]. Rac and Cdc42 are required for complex recruitment during FcγR phagocytosis, while Rho controls assembly at CR phagosomes [2, 3]. To better understand the role of in we tested idea that known target Rho, Rho-kinase (ROK), might control phagocytic cup formation and/or engulfment particles. Inhibitors ROK (dominant-negative Y-27632) downstream ROK, myosin-II (ML7, BDM, dominant-negative myosin-II), were used to test this idea. We found inhibition → caused decreased accumulation F-actin around bound particles, which led reduction CR-mediated engulfment. FcγR-mediated contrast, was independent activity only dependent on particle internalization, not formation. While myosins have been previously implicated phagocytosis [4–6], our knowledge, is first demonstration phagocytosis.