期刊
CELL CYCLE
卷 7, 期 11, 页码 1511-1521出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.7.11.5959
关键词
IAP; apoptosis; NF kappa B; TNF; c-IAP; NIK
类别
A family of anti-apoptotic regulators known as inhibitor of apoptosis (IAP) proteins block cell death in response to diverse stimuli. In spite of the fact that cellular IAP1and 2 (c-IAP1 and 2) were discovered more than 12 years ago, their physiological roles have remained obscure. Several molecular mechanisms were proposed to explain their anti-apoptotic activity, ranging from direct inhibition and ubiquitination of pro-apoptotic molecules, to the activation of pro-survival signaling. New findings present a surprising and complex twists. On the one hand, cIAP1 and c-IAP2 suppress Tumor Necrosis Factor alpha (TNF alpha) stimulated cell death by preventing formation of the TNF Receptor 1 (TNFR1) pro-apoptotic signaling complex. On the other hand, they regulate pro-survival NF kappa B signaling pathways: in the non- canonical pathway, by ubiquitination of NF kappa B-inducing kinase (NIK), and in the canonical pathway, by a yet-to-be- defined mechanism. In addition, c-IAPs self-regulate their protein levels through RING domain mediated auto-ubiquitination. Here, we discuss the most recent progress in our understanding of the biological roles of c-IAPs, as well as the implications of targeting c-IAPs for therapeutic intervention.
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