Induction of BIM, a proapoptotic BH3-only BCL-2 family member, is critical for neuronal apoptosis
- Author(s)
- Putcha, GV; Moulder, KL; Golden, JP; Bouillet, P; Adams, JA; Strasser, A; Johnson, EM;
- Details
- Publication Year 2001-03,Volume 29,Issue #3,Page 615-628
- Journal Title
- NEURON
- Publication Type
- Journal Article
- Abstract
- Sympathetic neuronal death induced by nerve growth factor (NGF) deprivation requires the macromolecular synthesis-dependent translocation of BAX from the cytosol to mitochondria and its subsequent integration into the mitochondrial outer membrane, followed by BAX-mediated cytochrome c (cyt c) release. The gene products triggering this process remain unknown. Here, we report that BIM, a member of the BH3-only proapoptotic subfamily of the BCL-2 protein family, is one such molecule. NGF withdrawal induced expression of BIMEL, an integral mitochondrial membrane protein that functions upstream of (or in parallel with) the BAX/BCL-2 and caspase checkpoints. aim deletion conferred protection against developmental and induced neuronal apoptosis in both central and peripheral populations, but only transiently, suggesting that BIM-and perhaps other BH3-only proteins-serve partially redundant functions upstream of BAX-mediated cyt c release.
- Publisher
- CELL PRESS
- Keywords
- NERVE GROWTH-FACTOR; PROGRAMMED CELL-DEATH; TROPHIC-FACTOR DEPRIVATION; CEREBELLAR GRANULE CELLS; DEPENDENT SYMPATHETIC NEURONS; BAX-DEFICIENT MICE; CYTOCHROME-C; PHOSPHATIDYLINOSITOL 3-KINASE; PROTEIN-KINASE; TRANSCRIPTION FACTOR
- Publisher's Version
- https://doi.org/10.1016/S0896-6273(01)00238-0
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2001-03-01 12:00:00