USP11: A key regulator of cIAP2 stability and sensitivity to SMAC mimetics

Abstract

The critical function of cellular inhibitor of apoptosis proteins (cIAPs) in the protection of cancer cells from numerous apoptotic stimuli prompted the development of second mitochondria-derived activator of caspases (SMAC) mimetics. We recently addressed a novel survival pathway in which cIAP2 is induced by tumor necrosis factor-α and is stabilized by its specific deubiquitylase, USP11, rendering cells resistant to SMAC mimetics.