bcl-2 inhibits death of central neural cells induced by multiple agents.

DOI Web Site 17 Citations
  • L T Zhong
    Department of Neurology, University of California School of Medicine, Los Angeles 90024-1769.
  • T Sarafian
    Department of Neurology, University of California School of Medicine, Los Angeles 90024-1769.
  • D J Kane
    Department of Neurology, University of California School of Medicine, Los Angeles 90024-1769.
  • A C Charles
    Department of Neurology, University of California School of Medicine, Los Angeles 90024-1769.
  • S P Mah
    Department of Neurology, University of California School of Medicine, Los Angeles 90024-1769.
  • R H Edwards
    Department of Neurology, University of California School of Medicine, Los Angeles 90024-1769.
  • D E Bredesen
    Department of Neurology, University of California School of Medicine, Los Angeles 90024-1769.

Abstract

<jats:p>The protooncogene bcl-2, which has been implicated in B-cell lymphoma development, inhibits apoptosis due to growth factor withdrawal in some, but not all, hematopoietic cells. Recently we found that bcl-2 also inhibits apoptosis in PC12 pheochromocytoma cells. We now report that bcl-2 inhibits the death of a central neural cell line due to serum and growth factor withdrawal, the calcium ionophore A23187, glucose withdrawal, membrane peroxidation, and, in some cases, free radical-induced damage. This broad range of protective effects of BCL-2 protein suggests that BCL-2 may interact with a central step in neural cell death. Measurements of intracellular free calcium suggest that BCL-2 alters the transduction of neural death signals at a point distal to the rise in intracellular free calcium.</jats:p>

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