RIPK 抑制因子

Receptor-interacting serine/threonine kinases (RIPKs) are a family of kinases that play a critical role in regulating cell death, inflammation, and immune responses. RIPKs, particularly RIPK1 and RIPK3, are best known for their involvement in necroptosis, a form of programmed necrosis. They function by interacting with various receptors, such as tumor necrosis factor receptors (TNFRs), and are activated through complex signaling cascades involving ubiquitination and phosphorylation. Upon activation, RIPKs can either promote cell survival and inflammation via activation of NF-κB and MAPK pathways or induce cell death through the formation of a necrosome complex, particularly in the presence of caspase inhibition. Their ability to switch between pro-survival and pro-death pathways is critical for maintaining cellular homeostasis and responding to cellular stress and damage.

RIPK (Receptor-interacting serine/threonine kinase) inhibitors are a group of chemical compounds designed to modulate the activity of receptor-interacting serine/threonine kinases, a family of kinases crucial in various cellular signaling pathways. These kinases, particularly RIPK1, RIPK2, and RIPK3, are involved in the regulation of cell death, inflammation, and immune responses. RIPK inhibitors operate by targeting these kinases, thereby modulating their kinase activity. The development of RIPK inhibitors has advanced our understanding of kinase signaling pathways. By inhibiting specific kinases, these compounds help elucidate the roles of RIPKs in various cellular processes. For example, the inhibition of RIPK1 can provide insights into its role in NF-κB activation, a crucial factor in the inflammatory response and cell survival.