XIAP is a member of a family of proteins which inhibit apoptosis and act as mammalian cell-death suppressors. XIAP inhibits at least 2 members of the caspase family of cell-death proteases, caspase-3 and caspase-7. In addition, XIAP inhibits apoptosis induced by menadione, a potent inducer of free radicals, and ICE. Furthermore, XIAP can mediate protection of cells from apoptosis by utilizing both a JNK1 activation pathway that involves ILPIP and a caspase inhibition pathway that is independent of ILPIP. Disruption of the XIAP gene in human colon cancer cells can enhance sensitivity of these cells to exogenously added TRAIL suggesting that XIAP is a nonredundant modulator of TRAIL-mediated apoptosis.
The proinflammatory cytokine tumour necrosis factor-alpha (TNF-alpha) regulates immune responses, inflammation and programmed cell death (apoptosis). The ultimate fate of a cell exposed to TNF-alpha is determined by signal integration between its different effectors, including IkappaB kinase (IKK), c-Jun N-terminal
The inhibitor-of-apoptosis (IAP) family of genes has an evolutionarily conserved role in regulating programmed cell death in animals ranging from insects to humans. Ectopic expression of human IAP proteins can suppress cell death induced by a variety of stimuli, but
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