The proapoptotic BCL-2 family member BIM mediates motoneuron loss in a model of amyotrophic lateral sclerosis
- 18 May 2007
- journal article
- research article
- Published by Springer Nature in Cell Death & Differentiation
- Vol. 14 (7) , 1386-1389
- https://doi.org/10.1038/sj.cdd.4402166
Abstract
No abstract availableKeywords
This publication has 20 references indexed in Scilit:
- ALS: A Disease of Motor Neurons and Their Nonneuronal NeighborsNeuron, 2006
- Molecular biology of amyotrophic lateral sclerosis: insights from geneticsNature Reviews Neuroscience, 2006
- Complete Dissociation of Motor Neuron Death from Motor Dysfunction by Bax Deletion in a Mouse Model of ALSJournal of Neuroscience, 2006
- Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALSMolecular and Cellular Neuroscience, 2006
- Impaired Extracellular Secretion of Mutant Superoxide Dismutase 1 Associates with Neurotoxicity in Familial Amyotrophic Lateral SclerosisJournal of Neuroscience, 2005
- Cell Death: Critical Control PointsPublished by Elsevier ,2004
- Loss of pro-apoptotic BH3-only Bcl-2 family member bim does not protect mutantLurcher mice from neurodegenerationJournal of Neuroscience Research, 2003
- JNK-Mediated BIM Phosphorylation Potentiates BAX-Dependent ApoptosisNeuron, 2003
- Nerve Growth Factor (NGF) Down-regulates the Bcl-2 Homology 3 (BH3) Domain-only Protein Bim and Suppresses Its Proapoptotic Activity by PhosphorylationJournal of Biological Chemistry, 2002
- Functional Role of Caspase-1 and Caspase-3 in an ALS Transgenic Mouse ModelScience, 2000