Deficiency or inhibition of oxygen sensor Phd1 induces hypoxia tolerance by reprogramming basal metabolism. - Wikidata - wikimedia - TriplyDB

Deficiency or inhibition of oxygen sensor Phd1 induces hypoxia tolerance by reprogramming basal metabolism.

Deficiency or inhibition of oxygen sensor Phd1 induces hypoxia tolerance by reprogramming basal metabolism.

http://www.wikidata.org/entity/Q42523283

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Hypoxia promotes glycogen accumulation through hypoxia inducible factor (HIF)-mediated induction of glycogen synthase 1 Selective inhibition of hypoxia-inducible factor (HIF) prolyl-hydroxylase 1 mediates neuroprotection against normoxic oxidative death via HIF- and CREB-independent pathways Metabolic insight into mechanisms of high-altitude adaptation in Tibetans Regulation of human metabolism by hypoxia-inducible factor Negative feedback control of HIF-1 through REDD1-regulated ROS suppresses tumorigenesis Adenosine and hypoxia-inducible factor signaling in intestinal injury and recovery Hypoxia-inducible factors and the response to hypoxic stress Mitochondrial metabolic remodeling in response to genetic and environmental perturbations Hypoxia Inducible Factor Pathway and Physiological Adaptation: A Cell Survival Pathway?Hypoxia-mediated regulation of macrophage functions in pathophysiology A conserved polybasic domain mediates plasma membrane targeting of Lgl and its regulation by hypoxia Hypoxia: an alarm signal during intestinal inflammation Molecular mechanisms of ischemic preconditioning in the kidney HIF prolyl hydroxylase inhibitors for anemia Redox regulation of mitochondrial function Oxygen sensing in Drosophila: multiple isoforms of the prolyl hydroxylase fatiga have different capacity to regulate HIFalpha/Sima Abnormal sympathoadrenal development and systemic hypotension in PHD3-/- mice Physical fitness and mitochondrial respiratory capacity in horse skeletal muscle Subcellular Energetics and Metabolism: A Cross-Species Framework.Subcellular Energetics and Metabolism: Potential Therapeutic Applications.Suppression of vascular network formation by chronic hypoxia and prolyl-hydroxylase 2 (phd2) deficiency during vertebrate development.Baf60c drives glycolytic metabolism in the muscle and improves systemic glucose homeostasis through Deptor-mediated Akt activation.Downregulation of miR-205 modulates cell susceptibility to oxidative and endoplasmic reticulum stresses in renal tubular cells.The ergogenic effect of recombinant human erythropoietin on VO2max depends on the severity of arterial hypoxemia.iTRAQ proteomic identification of pVHL-dependent and -independent targets of Egln1 prolyl hydroxylase knockdown in renal carcinoma cells.Hypoglycemia and the origin of hypoxia-induced reduction in human fetal growth.Double Knockdown of PHD1 and Keap1 Attenuated Hypoxia-Induced Injuries in Hepatocytes Hypoxia treatment reverses neurodegenerative disease in a mouse model of Leigh syndrome.Hearts of hypoxia-inducible factor prolyl 4-hydroxylase-2 hypomorphic mice show protection against acute ischemia-reperfusion injury HIF-1-mediated suppression of mitochondria electron transport chain function confers resistance to lidocaine-induced cell death.The ubiquitin ligase Siah2 and the hypoxia response.Prolyl hydroxylation by EglN2 destabilizes FOXO3a by blocking its interaction with the USP9x deubiquitinase.Prolyl Hydroxylase Domain-2 Inhibition Improves Skeletal Muscle Regeneration in a Male Murine Model of Obesity Endothelial HIF-2 mediates protection and recovery from ischemic kidney injury.The asparaginyl hydroxylase factor inhibiting HIF-1alpha is an essential regulator of metabolism Inhibition of hypoxia-inducible factor-targeting prolyl hydroxylase domain-containing protein 2 (PHD2) enhances matrix synthesis by human chondrocytes.Inhibition of prolyl hydroxylases by dimethyloxaloylglycine after stroke reduces ischemic brain injury and requires hypoxia inducible factor-1α.The Role of PPARα Activation in Liver and Muscle.Hemoglobin regulates the metabolic, synthetic, detoxification, and biotransformation functions of hepatoma cells cultured in a hollow fiber bioreactor.Renal cancer resistance to antiangiogenic therapy is delayed by restoration of angiostatic signaling.

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P2860

Deficiency or inhibition of oxygen sensor Phd1 induces hypoxia tolerance by reprogramming basal metabolism.

http://www.wikidata.org/entity/Q42523283

description

2008 nî lūn-bûn

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2008年の論文

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年學術文章

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name

Deficiency or inhibition of ox ...... eprogramming basal metabolism.

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Deficiency or inhibition of ox ...... eprogramming basal metabolism.

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type

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Deficiency or inhibition of ox ...... eprogramming basal metabolism.

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Deficiency or inhibition of ox ...... eprogramming basal metabolism.

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Deficiency or inhibition of ox ...... eprogramming basal metabolism.

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Nature Genetics

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Deficiency or inhibition of ox ...... eprogramming basal metabolism.

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Benedicte Jordan

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Bernard Gallez

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Bhathiya Wijeyekoon

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Carsten Willam

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Chris Pugh

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Christophe Deroose

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Florea Lupu

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Francis Sluse

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Frans Gorus

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Frans Schuit

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170-180

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scholarly article

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10.1038/NG.2007.62

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2

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40

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Peter Carmeliet

Peter J. Ratcliffe

Diether Lambrechts

Massimiliano Mazzone

Patrick H Maxwell

Alexandra Grosfeld

Antonio Diez-Juan

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2008-01-06T00:00:00Z

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5672849

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1025784046

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18176562

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