There are several endocytic pathways, which are either dependent on or independent of clathrin. This study focuses on a poorly characterized mechanism-clathrin-and caveolae-independent endocytosis-used by the interleukin-2 receptor b (IL-2Rb). We address the question of its regulation in comparison with the clathrin-dependent pathway. First, we show that Ras-related C3 botulinum toxin substrate 1 (Rac1) is specifically required for IL-2Rb entry, and we identify p21-activated kinases (Paks) as downstream targe…
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