The protooncogene bcl-2 inhibits apoptosis in PC12 cells.
During development, many neuronal populations undergo a process of normal, programmed cell death, or apoptosis. Trophic factors regulate this process, but the mechanism by which they suppress apoptosis remains unclear. In the immune system, recent studies have implicated the protooncogene bcl-2 in the lymphocyte survival response to growth factors. To determine whether a similar survival pathway exists in a neuroendocrine cell type, we have expressed bcl-2 in the rat pheochromocytoma PC12 cell line and found that it abrogates the requirement for stimulation by growth factors to survive. bcl-2 expression also substantially delays the onset of injury by the calcium ionophore A23187.
Mah
S P
SP
Department of Neurology, UCLA School of Medicine 90024-1769.
Zhong
L T
LT
Liu
Y
Y
Roghani
A
A
Edwards
R H
RH
Bredesen
D E
DE
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D000001:Calcimycin / Q000494:pharmacology; D002452:Cell Count / Q000187:drug effects; D002461:Cell Line, Transformed; D004273:DNA, Neoplasm / Q000378:metabolism; D006801:Humans; D010101:Oxygen Consumption / Q000187:drug effects; D016716:PC12 Cells / Q000187:drug effects / Q000473:pathology*; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology*; D019253:Proto-Oncogene Proteins c-bcl-2
D004273:DNA, Neoplasm; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D000001:Calcimycin