The proapoptotic BCL-2 family member BIM mediates motoneuron loss in a model of amyotrophic lateral sclerosis

[1]  J. Hsieh,et al.  Hierarchical regulation of mitochondrion-dependent apoptosis by BCL-2 subfamilies , 2006, Nature Cell Biology.

[2]  D. Cleveland,et al.  ALS: A Disease of Motor Neurons and Their Nonneuronal Neighbors , 2006, Neuron.

[3]  Robert H. Brown,et al.  Molecular biology of amyotrophic lateral sclerosis: insights from genetics , 2006, Nature Reviews Neuroscience.

[4]  R. Oppenheim,et al.  Complete Dissociation of Motor Neuron Death from Motor Dysfunction by Bax Deletion in a Mouse Model of ALS , 2006, The Journal of Neuroscience.

[5]  J. Julien,et al.  Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALS , 2006, Molecular and Cellular Neuroscience.

[6]  S. Korsmeyer,et al.  Bax Channel Inhibitors Prevent Mitochondrion-mediated Apoptosis and Protect Neurons in a Model of Global Brain Ischemia* , 2005, Journal of Biological Chemistry.

[7]  A. Hill,et al.  Impaired Extracellular Secretion of Mutant Superoxide Dismutase 1 Associates with Neurotoxicity in Familial Amyotrophic Lateral Sclerosis , 2005, The Journal of Neuroscience.

[8]  A. Saito,et al.  The c-Jun N-Terminal Protein Kinase Signaling Pathway Mediates Bax Activation and Subsequent Neuronal Apoptosis through Interaction with Bim after Transient Focal Cerebral Ischemia , 2004, The Journal of Neuroscience.

[9]  Robert H. Brown,et al.  Amyotrophic Lateral Sclerosis-Associated SOD1 Mutant Proteins Bind and Aggregate with Bcl-2 in Spinal Cord Mitochondria , 2004, Neuron.

[10]  S. Korsmeyer,et al.  Cell Death Critical Control Points , 2004, Cell.

[11]  A. Strasser,et al.  Loss of pro‐apoptotic BH3‐only Bcl‐2 family member bim does not protect mutant Lurcher mice from neurodegeneration , 2003, Journal of neuroscience research.

[12]  Eugene M. Johnson,et al.  JNK-Mediated BIM Phosphorylation Potentiates BAX-Dependent Apoptosis , 2003, Neuron.

[13]  L. Greene,et al.  Nerve Growth Factor (NGF) Down-regulates the Bcl-2 Homology 3 (BH3) Domain-only Protein Bim and Suppresses Its Proapoptotic Activity by Phosphorylation* , 2002, The Journal of Biological Chemistry.

[14]  M. Dubois‐Dauphin,et al.  Delaying Caspase Activation by Bcl-2: A Clue to Disease Retardation in a Transgenic Mouse Model of Amyotrophic Lateral Sclerosis , 2000, The Journal of Neuroscience.

[15]  J. Loeffler,et al.  Alteration of the Bcl-x/Bax Ratio in a Transgenic Mouse Model of Amyotrophic Lateral Sclerosis: Evidence for the Implication of the p53 Signaling Pathway , 2000, Neurobiology of Disease.

[16]  P. Stieg,et al.  Functional role of caspase-1 and caspase-3 in an ALS transgenic mouse model. , 2000, Science.

[17]  A. Hottinger,et al.  Increased motoneuron survival and improved neuromuscular function in transgenic ALS mice after intraspinal injection of an adeno-associated virus encoding Bcl-2. , 2000, Human molecular genetics.

[18]  A. Strasser,et al.  The proapoptotic activity of the Bcl-2 family member Bim is regulated by interaction with the dynein motor complex. , 1999, Molecular cell.

[19]  M. Dubois‐Dauphin,et al.  Bcl-2: prolonging life in a transgenic mouse model of familial amyotrophic lateral sclerosis. , 1997, Science.