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Sci. STKE, 18 October 2005
Vol. 2005, Issue 306, p. re12
[DOI: 10.1126/stke.3062005re12]

REVIEWS

Integration of Oxygen Signaling at the Consensus HRE

Roland H. Wenger*, Daniel P. Stiehl, and Gieri Camenisch

Institute of Physiology and Center for Integrative Human Physiology (CIHP), University of Zürich, CH-8057 Zürich, Switzerland.

Gloss: Oxygen availability regulates many physiological and pathophysiological processes, including embryonic development, high-altitude adaptation, wound healing, and inflammation, as well as contributing to the pathophysiology of ischemic diseases and cancer. Central to our understanding of these processes is an elucidation of the molecular mechanisms by which cells react and adapt to insufficient oxygen supply (hypoxia). The last few years have brought a wealth of novel insights into these processes. Oxygen-sensing protein hydroxylases have been discovered that regulate the abundance and activity of three hypoxia-inducible transcription factors (HIFs) and thereby the activity of at least 70 effector genes involved in hypoxic adaptation. In addition to the increase in HIF abundance in response to a decrease in tissue oxygenation, it became evident that HIF abundance is also proactively increased, even under normoxic conditions, in response to stimuli that lead to cell growth and thus ultimately require higher oxygen consumption. The growing cell thus profits from an anticipatory increase in HIF-dependent target gene expression. Growth stimuli–activated signaling pathways that influence the abundance and activity of HIFs include pathways that involve the activation of kinases and liberation of reactive oxygen species. All of these pathways converge at the hypoxia-response elements (HREs) of effector genes, to which the HIFs bind, thereby enabling HIF-dependent induction of gene expression.

*Corresponding author. Institute of Physiology and Center for Integrative Human Physiology (CIHP), University of Zürich-Irchel, Winterthurerstrasse 190, CH-8057 Zürich, Switzerland. E-Mail: roland.wenger{at}access.unizh.ch

Citation: R. H. Wenger, D. P. Stiehl, G. Camenisch, Integration of Oxygen Signaling at the Consensus HRE. Sci. STKE 2005, re12 (2005).


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   Abstract »    Full Text »    PDF »
Hypoxia Up-Regulates Hypoxia-Inducible Factor-1{alpha} Transcription by Involving Phosphatidylinositol 3-Kinase and Nuclear Factor {kappa}B in Pulmonary Artery Smooth Muscle Cells.
R. S. BelAiba, S. Bonello, C. Zahringer, S. Schmidt, J. Hess, T. Kietzmann, and A. Gorlach (2007)
Mol. Biol. Cell 18, 4691-4697
   Abstract »    Full Text »    PDF »
Oxygen-dependent ATF-4 stability is mediated by the PHD3 oxygen sensor.
J. Koditz, J. Nesper, M. Wottawa, D. P. Stiehl, G. Camenisch, C. Franke, J. Myllyharju, R. H. Wenger, and D. M. Katschinski (2007)
Blood 110, 3610-3617
   Abstract »    Full Text »    PDF »
From critters to cancers: bridging comparative and clinical research on oxygen sensing, HIF signaling, and adaptations towards hypoxia.
D. Hoogewijs, N. B. Terwilliger, K. A. Webster, J. A. Powell-Coffman, S. Tokishita, H. Yamagata, T. Hankeln, T. Burmester, K. T. Rytkonen, M. Nikinmaa, et al. (2007)
Integr. Comp. Biol. 47, 552-577
   Abstract »    Full Text »    PDF »
Myocardial hypoxia-inducible HIF-1{alpha}, VEGF, and GLUT1 gene expression is associated with microvascular and ICAM-1 heterogeneity during endotoxemia.
R. M. Bateman, C. Tokunaga, T. Kareco, D. R. Dorscheid, and K. R. Walley (2007)
Am J Physiol Heart Circ Physiol 293, H448-H456
   Abstract »    Full Text »    PDF »
Hypoxia-inducible Factor-1 (HIF-1) Is a Transcriptional Activator of the TrkB Neurotrophin Receptor Gene.
L. K. Martens, K. M. Kirschner, C. Warnecke, and H. Scholz (2007)
J. Biol. Chem. 282, 14379-14388
   Abstract »    Full Text »    PDF »
Glycogen Synthase Kinase 3 Phosphorylates Hypoxia-Inducible Factor 1{alpha} and Mediates Its Destabilization in a VHL-Independent Manner.
D. Flugel, A. Gorlach, C. Michiels, and T. Kietzmann (2007)
Mol. Cell. Biol. 27, 3253-3265
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Reactive Oxygen Species Activate the HIF-1{alpha} Promoter Via a Functional NF{kappa}B Site.
S. Bonello, C. Zahringer, R. S. BelAiba, T. Djordjevic, J. Hess, C. Michiels, T. Kietzmann, and A. Gorlach (2007)
Arterioscler Thromb Vasc Biol 27, 755-761
   Abstract »    Full Text »    PDF »
Glucose-Stimulated Insulin Production in Mice Deficient for the PAS Kinase PASKIN.
E. Borter, M. Niessen, R. Zuellig, G. A. Spinas, P. Spielmann, G. Camenisch, and R. H. Wenger (2007)
Diabetes 56, 113-117
   Abstract »    Full Text »    PDF »
Translational Control of Collagen Prolyl 4-Hydroxylase-{alpha}(I) Gene Expression under Hypoxia.
M. Fahling, R. Mrowka, A. Steege, G. Nebrich, A. Perlewitz, P. B. Persson, and B. J. Thiele (2006)
J. Biol. Chem. 281, 26089-26101
   Abstract »    Full Text »    PDF »
Hypoxia Modifies the Transcriptome of Primary Human Monocytes: Modulation of Novel Immune-Related Genes and Identification Of CC-Chemokine Ligand 20 as a New Hypoxia-Inducible Gene.
M. C. Bosco, M. Puppo, C. Santangelo, L. Anfosso, U. Pfeffer, P. Fardin, F. Battaglia, and L. Varesio (2006)
J. Immunol. 177, 1941-1955
   Abstract »    Full Text »    PDF »

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