RIPK1, RIPK3 and MLKL are the main molecules involved in necroptosis. The kinase activity of RIPK1 is essential for many complexes. IAP-induced ubiquitination of RIPK1 leads to NF-κB activation and subsequent inflammation cascades. The inhibition of caspase-8 activity caused by FLIP can prevent RIPK1 from cleavage and drive necroptosis. Necrostatin-1 (Nec-1) is a small molecule that has been reported to inhibit the activity of RIP1K. The inhibition of necroptosis has been observed in the presence of necrostatin-1. Toll-like receptors (TLR) activate necroptosis through the interaction of TRIF and necrosomes. Necroptosis plays an important role in cancer and several neurodegenerative diseases. Studying the mechanisms of necroptosis and other cell death pathways can provide valuable insights for the development of new treatments for various diseases.
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