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   <subfield code="a">Signaling by reactive oxygen species in the nervous system</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[P. Maher*, D. Schubert]</subfield>
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   <subfield code="a">Abstract.: Free radicals and reactive oxygen species (ROS) are involved in a variety of different cellular processes ranging from apoptosis and necrosis to cell proliferation and carcinogenesis. Cells contain multiple sites for ROS production and a few mechanisms for their degradation. Which of these sites is activated by a given stimulus may play a role in dictating the subsequent downstream effects of the ROS generated on cellular function. Even when the ultimate outcome is similar, such as when ROS production leads to cell death, the specific cellular changes can be quite different depending on the initial stimulus and the type of cell involved. These data, along with the evidence that ROS can modify a number of intracellular signaling pathways including protein phosphatases, protein kinases and transcription factors, suggest that the majority of the effects of ROS on cells are through their actions on signaling pathways rather than via nonspecific damage of intracellular macromolecules.</subfield>
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   <subfield code="a">Birkhäuser Verlag Basel,, 2000</subfield>
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   <subfield code="a">Key words. ROS</subfield>
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   <subfield code="a">apoptosis</subfield>
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   <subfield code="a">necrosis</subfield>
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   <subfield code="a">glutathione</subfield>
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   <subfield code="a">H2O2</subfield>
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   <subfield code="a">tyrosine phosphatases</subfield>
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   <subfield code="u">The Scripps Research Institute, Department of Cell Biology, 10550 N. Torrey Pines Rd., La Jolla (California 92037, USA), Fax +1 858 784 7675, e-mail: pmaher@scripps.edu, US</subfield>
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