The PHD1 oxygen sensor in health and disease
Author:
Affiliation:
1. Department of General, Visceral and Transplantation Surgery; University of Heidelberg; Heidelberg Germany
2. UCD Conway Institute & School of Medicine; University College Dublin; Belfield Dublin 4 Ireland
Funder
European Union
Science Foundation Ireland
Deutsche Krebshilfe
Publisher
Wiley
Subject
Physiology
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1113/JP275327/fullpdf
Reference111 articles.
1. Disruption of hypoxia-inducible transcription factor-prolyl hydroxylase domain-1 (PHD-1−/−) attenuates ex vivo myocardial ischemia/reperfusion injury through hypoxia-inducible factor-1α transcription factor and its target genes in mice;Adluri;Antioxid Redox Signal,2011
2. Overexpression of the HIF hydroxylases PHD1, PHD2, PHD3 and FIH are individually and collectively unfavorable prognosticators for NSCLC survival;Andersen;PLoS One,2011
3. Differential function of the prolyl hydroxylases PHD1, PHD2, and PHD3 in the regulation of hypoxia-inducible factor;Appelhoff;J Biol Chem,2004
4. Regulation of HIF prolyl hydroxylases by hypoxia-inducible factors;Aprelikova;J Cell Biochem,2004
5. Deficiency or inhibition of oxygen sensor Phd1 induces hypoxia tolerance by reprogramming basal metabolism;Aragones;Nat Genet,2008
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