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This Week in Science plays a pivotal role in the cellular response to low oxygen levels; its activation under hypoxic conditions leads to increased transcription of genes implicated in O2 delivery and adaptive responses to O2 deprivation. Hagen et al. (p. 1975) now find that HIF1 is destabilized by nitric oxide (NO) and other inhibitors of mitochondrial respiration by an increase in HIF1 degradation triggered by increased activity of the O2 -dependent enzyme prolyl hydroxylase. This NO-mediated inhibition of mitochondrial O2 consumption may increase O2 availability for nonrespiratory functions (such as prolyl hydroxylases) and cause the cell to fail to register hypoxia. Thus, redistribution of intracellular O2 may be another important consequence of NO action.
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Science. ISSN 0036-8075 (print), 1095-9203 (online)
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