PELI1 Selectively Targets Kinase-Active RIP3 for Ubiquitylation-Dependent Proteasomal Degradation (Molecular Cell)

Choi et al. show that PELI1-mediated K48-linked polyubiquitylation of kinase-active RIP3 leads to its proteasome-dependent degradation. Regulation of activated RIP3 by PELI1 provides a homeostatic mechanism to prevent aberrant cell death and minimize necroptotic pathology that occurs in diseases such as toxic epidermal necrolysis.