The Combination of Bcl-2 Expression and NGF-Deprivation Facilitates the Selective Destruction of BAD Protein in Living Sympathetic Neurons
- 1 August 2000
- journal article
- Published by Elsevier in Molecular and Cellular Neuroscience
- Vol. 16 (2) , 97-110
- https://doi.org/10.1006/mcne.2000.0867
Abstract
No abstract availableKeywords
This publication has 52 references indexed in Scilit:
- A Role for MAPK/ERK in Sympathetic Neuron Survival: Protection against a p53-Dependent, JNK-Independent Induction of Apoptosis by Cytosine ArabinosideJournal of Neuroscience, 1999
- Phosphatidylinositol 3-Kinase and Akt Protein Kinase Are Necessary and Sufficient for the Survival of Nerve Growth Factor-Dependent Sympathetic NeuronsJournal of Neuroscience, 1998
- Akt Phosphorylation of BAD Couples Survival Signals to the Cell-Intrinsic Death MachineryCell, 1997
- Bcl-2 promotes regeneration of severed axons in mammalian CNSNature, 1997
- BAX Is Required for Neuronal Death after Trophic Factor Deprivation and during DevelopmentNeuron, 1996
- Mitogen-activated Protein Kinase-independent Pathways Mediate the Effects of Nerve Growth Factor and cAMP on Neuronal SurvivalJournal of Biological Chemistry, 1996
- bcl-2 overexpression reduces apoptotic photoreceptor cell death in three different retinal degenerations.Proceedings of the National Academy of Sciences, 1996
- Protection of Retinal Ganglion Cells from Natural and Axotomy-Induced Cell Death in Neonatal Transgenic Mice Overexpressing bcl-2Journal of Neuroscience, 1996
- Role of Bcl‐2 in the Brain‐derived Neurotrophic Factor Survival ResponseEuropean Journal of Neuroscience, 1995
- The proto-oncogene bcl-2 can selectively rescue neurotrophic factor-dependent neurons from apoptosisCell, 1993