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Howard Hughes Medical Institute, Departments of Medicine and Biochemistry, Duke University Medical Center, Durham, North Carolina 27710, USA
1Correspondence: Room 321, MSRB, DUMC 2612, Duke University Medical Center, Durham, NC 27710, USA. E-mail STAML001{at}mc.duke.edu
A growing body of evidence suggests that the cellular response to
oxidative and nitrosative stress is primarily regulated at the level of
transcription. Posttranslational modification of transcription factors
may provide a mechanism by which cells sense these redox changes. In
bacteria, for example, OxyR senses redox-related changes via oxidation
or nitrosylation of a free thiol in the DNA binding region. This mode
of regulation may serve as a paradigm for redox-sensing by eukaryotic
transcription factors as most—including NF-
B, AP-1, and
p53—contain reactive thiols in their DNA binding regions, the
modification of which alters binding in vitro. Several
of these transcription factors have been found to be sensitive to both
reactive oxygen species and nitric oxide-related species in
vivo. It remains entirely unclear, however, if oxidation or
nitrosylation of eukaryotic transcription factors is an important mode
of regulation, or whether transcriptional activating pathways are
principally controlled at other redox-sensitive levels.—Marshall,
H. E., Merchant, K., Stamler, J. S. Nitrosation and oxidation
in the regulation of gene expression.
Key Words: nitric oxide • oxidative stress • nitrosative stress • S-nitrosylation • thiols • transcription factors
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