Bcl2 inhibits apoptosis associated with terminal differentiation of HL- 60 myeloid leukemia cells
作者： L Naumovski , ML Cleary
DOI: 10.1182/BLOOD.V83.8.2261.2261
关键词:
摘要: The Bcl2 protein inhibits apoptosis (programmed cell death) induced by a variety of noxious stimuli. However, relatively little is known about its effect on that occurs after terminal differentiation. levels decrease during differentiation myeloid cells into granulocytes subsequently undergo apoptosis, but the potential role in coupling survival and remains undefined. To ascertain relationship between decreasing onset differentiating cells, was hyperexpressed HL-60 line retroviral gene transfer. After treatment HL-60/BCL2 with all-trans retinoic acid or phorbol myristic acid, did not as normal but, rather, increased because activation viral promoter. Differentiation Bcl2-overexpressing similar to they showed evidence for had prolonged survival. These studies show survival-enhancing properties counteract programmed death accompanies differentiation; however, has no significant itself, suggesting are regulated independently cells.
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