Abstract
Apoptosis and clearance of dead cells is highly evolutionarily conserved from nematode to humans, which is crucial to the growth and development of multicellular organism. Fail to remove apoptotic cells often lead to homeostasis imbalance, fatal autoimmune diseases, and neurodegenerative diseases. Small ubiquitin-related modifiers (SUMOs) modification is a post-translational modification of ubiquitin proteins mediated by the sentrin-specific proteases (SENPs) family. SUMO modification is widely involved in many cellular biological process, and abnormal SUMO modification is also closely related to many major human diseases. Recent researches have revealed that SUMO modification event occurs during apoptosis and clearance of apoptotic cells, and plays an important role in the regulation of apoptotic signaling pathways. This review summarizes some recent progress in the revelation of regulatory mechanisms of these pathways and provides some potential researching hotpots of the SUMO modification regulation to apoptosis.
Highlights
Apoptosis is an evolutionarily conserved cell progress from nematode to mammals, which is of great importance for organisms normal development, failure to apoptotic cells clearance can result in the release of toxins and inflammation of the surrounding environment (Elliott and Ravichandran 2010; Munoz et al 2005)
We briefly describe the process of cell death and the SUMOylation discuss the relationship between apoptosis and ubiquitination-like modification
Apoptotic cells are swiftly phagocytosed by macrophages to prevent the release of intracellular components, timely and effective elimination of apoptotic cells can prevent the body from producing inflammation or autoimmune diseases
Summary
Apoptosis is an evolutionarily conserved cell progress from nematode to mammals, which is of great importance for organisms normal development, failure to apoptotic cells clearance can result in the release of toxins and inflammation of the surrounding environment (Elliott and Ravichandran 2010; Munoz et al 2005). TNFR1-associated death domain protein (TRADD) does not directly activate caspase-8, but it can serve as a membrane-binding scaffold for additional signaling molecules, including kinases, receptor interaction protein 1 (RIP1), and ubiquitin-ligases TRAF2 and cIAP1/2. CED-1 interacts with CED-6 to recruit clathrin CHC-1 and the multi-subunit adaptor protein AP2, forming a complex to mediate actin cytoskeleton rearrangement (Chen et al 2013b); on the other hand, AP2 interact with LST-4 and DYN-1 to initiate the cell intima into the "phagocytic cup", subsequently causes cytoskeletal rearrangement and promotes the extension of phagocytic pseudopodia (Yu et al 2006) Another pathway that controls the phagocytosis of apoptotic cells by adjacent cells is composed of CED-2, CED-5, CED-10, CED12, and PSR-1 (Hsu and Wu 2010). SUMO’s connection to the substrate requires a series of enzymatic cascades, including E1 activase (Sae1/Sae heterodimer in humans), E2 conjugating enzyme (Ubc in humans), and E3 ligase
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