Journal article
BAX Is Required for Neuronal Death after Trophic Factor Deprivation and during Development
Neuron (Cambridge, Mass.), Vol.17(3), pp.401-411
1996
DOI: 10.1016/S0896-6273(00)80173-7
PMID: 8816704
Abstract
Members of the BCL2-related family of proteins either promote or repress programmed cell death. BAX, a death-promoting member, heterodimerizes with multiple death-repressing molecules, suggesting that it could prove critical to cell death. We tested whether
Bax is required for neuronal death by trophic factor deprivation and during development. Neonatal sympathetic neurons and facial motor neurons from
Bax-deficient mice survived nerve growth factor deprivation and disconnection from their targets by axotomy, respectively. These salvaged neurons displayed remarkable soma atrophy and reduced elaboration of neurites; yet they responded to readdition of trophic factor with soma hypertrophy and enhanced neurite outgrowth.
Bax-deficient superior cervical ganglia and facial nuclei possessed increased numbers of neurons. Our observations demonstrate that trophic factor deprivation–induced death of sympathetic and motor neurons depends on
Bax.
Details
- Title: Subtitle
- BAX Is Required for Neuronal Death after Trophic Factor Deprivation and during Development
- Creators
- Thomas L Deckwerth - Department of Molecular Biology and Pharmacology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, Missouri 63110, USAJeffrey L Elliott - Department of Neurology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, Missouri 63110, USAC.Michael Knudson - Department of Medicine and Pathology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, Missouri 63110, USAEugene M Johnson - Department of Molecular Biology and Pharmacology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, Missouri 63110, USAWilliam D Snider - Department of Neurology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, Missouri 63110, USAStanley J Korsmeyer - Department of Medicine and Pathology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, Missouri 63110, USA
- Resource Type
- Journal article
- Publication Details
- Neuron (Cambridge, Mass.), Vol.17(3), pp.401-411
- Publisher
- Elsevier Inc
- DOI
- 10.1016/S0896-6273(00)80173-7
- PMID
- 8816704
- ISSN
- 0896-6273
- eISSN
- 1097-4199
- Language
- English
- Date published
- 1996
- Academic Unit
- Pathology; Radiation Oncology
- Record Identifier
- 9984047730102771
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