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JNCI Journal of the National Cancer Institute 1999 91(2):106-107; doi:10.1093/jnci/91.2.106
© 1999 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 91, No. 2, 106-107, January 20, 1999
© 1999 Oxford University Press

EDITORIALS

aHIF: the Missing Link Between HIF-1 and VHL?

Leonard M. Neckers

Affiliation of author: L. M. Neckers, Cell and Cancer Biology Department, Medicine Branch, Division of Clinical Sciences, National Cancer Institute, Bethesda, MD.

Correspondence to: Leonard M. Neckers, Ph.D., National Institutes of Health, 9610 Medical Center Drive, Suite 300, Rockville, MD 20850 (e-mail: len@helix.nih.gov).

Response to hypoxia at the cellular level is composed of two components. Investigation of erythropoietin (EPO) gene regulation led to the discovery several years ago of a novel, hypoxia-inducible transcription factor, called hypoxia-inducible factor-1 (HIF-1), that stimulates transcription of a number of cellular hypoxia-survival genes, including EPO, vascular endothelial growth factor (VEGF), certain glycolytic enzymes, and the glucose transport protein GLUT-1. HIF-1 itself is heterodimeric, consisting of a constitutively expressed subunit (HIF-1ß or ARNT [aryl hydrocarbon nuclear translocator protein]) and a hypoxia-inducible subunit (HIF-1{alpha}). Hypoxia appears to regulate HIF-1{alpha} not at the transcriptional level but by post-transcriptional protein stabilization (1).

The second component of the cellular response to hypoxia involves the stabilization of certain messenger RNAs (mRNAs), usually the very ones whose genes are transcriptionally activated . . . [Full Text of this Article]

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