NSE-bcl-2 transgenic mice, a model system for studying neuronal death and survival
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Bernard, R
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ROYAL MELBOURNE HOSP,WALTER & ELIZA HALL INST MED RES,PARKVILLE,VIC 3050,AUSTRALIAROYAL MELBOURNE HOSP,WALTER & ELIZA HALL INST MED RES,PARKVILLE,VIC 3050,AUSTRALIA
Bernard, R
[1
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Farlie, P
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ROYAL MELBOURNE HOSP,WALTER & ELIZA HALL INST MED RES,PARKVILLE,VIC 3050,AUSTRALIAROYAL MELBOURNE HOSP,WALTER & ELIZA HALL INST MED RES,PARKVILLE,VIC 3050,AUSTRALIA
Farlie, P
[1
]
Bernard, O
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ROYAL MELBOURNE HOSP,WALTER & ELIZA HALL INST MED RES,PARKVILLE,VIC 3050,AUSTRALIAROYAL MELBOURNE HOSP,WALTER & ELIZA HALL INST MED RES,PARKVILLE,VIC 3050,AUSTRALIA
Bernard, O
[1
]
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[1] ROYAL MELBOURNE HOSP,WALTER & ELIZA HALL INST MED RES,PARKVILLE,VIC 3050,AUSTRALIA
Bcl-2 is a crucial regulator of cell survival and death. We have recently demonstrated that transgenic mice overexpressing the human Bcl-2 protein specifically in their neurons have an increased number of neuronal cells which can survive in tissue culture in the absence of neurotrophic factors. In order to understand why only some neurons can be rescued from developmental and neurotrophic factor deprivation-induced death, we have studied the expression pattern of the transgene during embryonic development and in adulthood. We have demonstrated that transgene expression starts in embryos at E12.5 and that only half of the sensory neurons of the dorsal root ganglia expressed detectable levels of the human Bcl-2. These results may explain why only 40% of the sensory neurons survived in tissue culture in the absence of neurotrophic factors.