AMP kinase–mediated activation of the BH3-only protein Bim couples energy depletion to stress-induced apoptosis
Open Access
- 29 March 2010
- journal article
- Published by Rockefeller University Press in The Journal of cell biology
- Vol. 189 (1), 83-94
- https://doi.org/10.1083/jcb.200909166
Abstract
Disturbances in cellular ion gradients by excitotoxicity promote apoptosis through activation of the Bcl-2 family member Bim.Keywords
This publication has 62 references indexed in Scilit:
- Pro-apoptotic Bim Induction in Response to Nerve Growth Factor Deprivation Requires Simultaneous Activation of Three Different Death Signaling PathwaysOnline Journal of Public Health Informatics, 2007
- Role of the JNK pathway in NMDA-mediated excitotoxicity of cortical neuronsCell Death & Differentiation, 2006
- Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell deathNature, 2005
- Cleavage of the Plasma Membrane Na+/Ca2+ Exchanger in ExcitotoxicityCell, 2005
- A peptide inhibitor of c-Jun N-terminal kinase protects against excitotoxicity and cerebral ischemiaNature Medicine, 2003
- Mitochondrial and extramitochondrial apoptotic signaling pathways in cerebrocortical neuronsProceedings of the National Academy of Sciences of the United States of America, 2000
- Proapoptotic Bcl-2 Relative Bim Required for Certain Apoptotic Responses, Leukocyte Homeostasis, and to Preclude AutoimmunityScience, 1999
- Glutamate-induced neuronal death: A succession of necrosis or apoptosis depending on mitochondrial functionNeuron, 1995
- Apoptosis and necrosis: two distinct events induced, respectively, by mild and intense insults with N-methyl-D-aspartate or nitric oxide/superoxide in cortical cell cultures.Proceedings of the National Academy of Sciences of the United States of America, 1995
- Inhibition of α2/α3 sodium pump isoforms potentiates glutamate neurotoxicityBrain Research, 1992