Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Sci. STKE, 16 December 2003
Vol. 2003, Issue 213, p. tw493
[DOI: 10.1126/stke.2132003tw493]



The transcription factor hypoxia-inducible factor (HIF) 1α 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. now find that HIF-1α is destabilized by nitric oxide (NO) and other inhibitors of mitochondrial respiration by an increase in HIF-1α 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 may cause the cell to fail to register hypoxia. Thus, redistribution of intracellular O2 may be another important consequence of NO action.

T. Hagen, C. T. Taylor, F. Lam, S. Moncada, Redistribution of intracellular oxygen in hypoxia by nitric oxide: Effect on HIF1α. Science 302, 1975-1978 (2003). [Abstract] [Full Text]

Citation: NO and Hypoxia. Sci. STKE 2003, tw493 (2003).

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882