For a model system, we study oxidative glutamate toxicity in a neuronal cell line. Previously, we determined several agents that are effective at preventing programmed cell death in this system, and during the past year, we characterized the mechanisms that underlie this protection. One agent that is effective is an activator of protein kinase C, a family of enzymes involved in a variety of cellular responses. We identified several different downstream signaling pathways that are critical for the protective effect of protein kinase C activation, indicating that the role of these enzymes in regulating programmed cell death may be quite complex. Never-theless, a greater understanding of this role could provide valuable therapeutic targets for preventing neuronal cell death.
C regulates glutamate-induced nerve cell death.
Maher, P.A. p38 map kinase activation is required for fibroblast growth factor-2 stimulated cell proliferation but not differentiation. Maher, P.A., Tan, S. Monoamines, monoamine oxidase inhibitors and the maintenance of mitochondrial function during oxidative stress. Marcel Dekker, New York, in press. Sagara, Y., Tan, S., Maher, P.A., Schubert, D. Mechanisms of resistance to oxidative stress in Alzheimer's disease. The regulation of reactive oxygen species production during programmed cell death.