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Antioxid Redox Signal. 2000 Fall;2(3):537-50.

Redox aspects of Bcl-2 function.

Author information

1
Department of Genetics, Stanford University School of Medicine, CA 94305-5318, USA. Voehringer@stanford.edu

Abstract

The oncogene Bcl-2 has attracted recent research attention as recognition of the importance of Bcl-2 control over apoptosis commitment in disease development and clinical response to therapy has been targeted for pharmacological intervention. Much of the basic science research regarding Bcl-2 has focused on the role that Bcl-2 plays in directly regulating mitochondrial function. This has come about because of Bcl-2's localization to mitochondrial membranes and its reported interaction with the mitochondrial megachannel. During the time that the mitochondrial function of Bcl-2 was being investigated, a smaller, yet potentially as important, role for Bcl-2 was being pursued by investigators who were following up the initial study of Bcl-2 knockout mice. These mice expressed a phenotype consistent with that of mice exposed to chronic oxidative stress. This research into the redox aspects of Bcl-2 function has led to a hypothesis that Bcl-2-expressing cells have enhanced antioxidant capacities that suppress oxidative stress signals generated during the initiation phase of many apoptotic pathways. This review will further develop the idea of Bcl-2's role in regulating cellular redox pathways associated with apoptosis, as well as integrate recently reported evidence that ties the antioxidant effects of Bcl-2 to mitochondrial function, thereby unifying both mitochondrial and redox aspects of Bcl-2 function.

PMID:
11229367
DOI:
10.1089/15230860050192314
[Indexed for MEDLINE]

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