Abstract
TNF receptor‐1 (TNFR1) and TRAIL death receptors preferentially induce pro‐inflammatory or cytotoxic signaling, respectively, via distinct plasma membrane and cytosolic complexes. New studies identifying the pro‐inflammatory factors TRAF2, RIP, and LUBAC in TRAIL death receptor complexes suggest that the latter are more “TNFR1‐like” than anticipated and argue for revision of prevailing models of spatio‐hierarchical TRAIL‐induced signaling complex assembly.
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