Prevention of programmed cell death of sympathetic neurons by the bcl-2 proto-oncogene.
Approximately half of the neurons produced during embryogenesis normally die before adulthood. Although target-derived neurotrophic factors are known to be major determinants of programmed cell death--apoptosis--the molecular mechanisms by which trophic factors interfere with cell death regulation are largely unknown. Overexpression of the bcl-2 proto-oncogene in cultured sympathetic neurons has now been shown to prevent apoptosis normally induced by deprivation of nerve growth factor. This finding, together with the previous demonstration of bcl-2 expression in the nervous system, suggests that the Bcl-2 protein may be a major mediator of the effects of neurotrophic factors on neuronal survival.
Garcia
I
I
Department of Pathology, Centre Médical Universitaire, Geneva, Switzerland.
Martinou
I
I
Tsujimoto
Y
Y
Martinou
J C
JC
D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D016923:Cell Death / Q000235:genetics*; D002478:Cells, Cultured; D005728:Ganglia, Sympathetic / Q000166:cytology; D015870:Gene Expression; D006801:Humans; D009414:Nerve Growth Factors / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D019253:Proto-Oncogene Proteins c-bcl-2; D051381:Rats; D013564:Sympathetic Nervous System / Q000166:cytology*; D014162:Transfection
C000715470:MAS1 protein, human; D009414:Nerve Growth Factors; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2