Regulation of cell death protease caspase-9 by phosphorylation.
Placement of the BCL2 family member BAX in the death pathway of sympathetic neurons activated by trophic factor deprivation. Expression of a murine homologue of the inhibitor of apoptosis protein is related to cell proliferation. Kobayashi, K., Hatano, M., Otaki, M., Ogasawara, T. A single BIR domain of XIAP sufficient for inhibiting caspases. Suppression of apoptosis in mammalian cells by NAIP and a related family of IAP genes. Adenovirus-mediated gene transfer of inhibitors of apoptosis protein delays apoptosis in cerebellar granule neurons. Phosphatidylinositol 3-kinase and Akt protein kinase are necessary and sufficient for the survival of nerve growth factor-dependent sympathetic neurons. Is activation of the Na +K + pump necessary for NGF-mediated neuronal survival. IAP family proteins-suppressors of apoptosis.
The iap genes: unique arbitrators of cell death. The TNFR2-TRAF signaling complex contains two novel proteins related to baculoviral inhibitor of apoptosis proteins. Cloning and expression of apoptosis inhibitory protein homologues that function to inhibit apoptosis and/or bind tumor necrosis factor receptor-associated factors. A conserved family of cellular genes related to the baculovirus iap gene and encoding apoptosis inhibitors. ITA, a vertebrate homologue of IAP that is expressed in T lymphocytes. The c-IAP-1 and c-IAP-2 proteins are direct inhibitors of specific caspases. X-linked IAP is a direct inhibitor of cell-death proteases. Caspase-9 can be activated without proteolytic processing. Ordering the cytochrome c-initiated caspase cascade: Hierarchical activation of caspases-2, -3, -6, -7, -8, and -10 in a caspase-9- dependent manner.
IAPs block apoptotic events induced by caspase-8 and cytochrome c by direct inhibition of distinct caspases.
Evidence of a novel event during neuronal death: development of competence-to-die in response to cytoplasmic cytochrome c. BAX is required for neuronal death after trophic factor deprivation and during development. Bax-deficient mice with lymphoid hyperplasia and male germ cell death. Programmed cell death in neurons: focus on the pathway of nerve growth factor deprivation-induced death of sympathetic neurons. Functions of the neurotrophins during nervous system development: What the knockouts are teaching us. Mice lacking nerve growth factor display perinatal loss of sensory and sympathetic neurons yet develop basal forebrain cholinergic neurons.
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