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Circulation Research, ISSN 0009-7330, 06/2015, Volume 117, Issue 1, pp. 65 - 79
Hypoxia inducible factors (HIFs) are α/β heterodimeric transcription factors that direct multiple cellular and systemic responses in response to changes in... 
hypoxia | dioxygenases | prolyl hydroxylases | hypoxia inducible factor | CARDIAC OUTFLOW TRACT | CARDIAC & CARDIOVASCULAR SYSTEMS | MYOCARDIAL-INFARCTION | PULMONARY ARTERIAL-HYPERTENSION | HYPOXIA-INDUCIBLE-FACTOR | FACTOR-I | ISCHEMIA-REPERFUSION INJURY | GENE-ENVIRONMENT INTERACTION | HIGH-ALTITUDE ADAPTATION | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | CAROTID-BODY | HEMATOLOGY | Adaptation, Physiological | Polycythemia - genetics | Heart Defects, Congenital - embryology | Cardiovascular Diseases - drug therapy | Heart - embryology | Humans | Hypoxia-Inducible Factor-Proline Dioxygenases - antagonists & inhibitors | Cardiovascular Diseases - enzymology | Oxygen - metabolism | Hypoxia - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - deficiency | Hypoxia-Inducible Factor-Proline Dioxygenases - deficiency | Cell Hypoxia | Repressor Proteins - physiology | Basic Helix-Loop-Helix Transcription Factors - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Heart Defects, Congenital - enzymology | Von Hippel-Lindau Tumor Suppressor Protein - genetics | Mixed Function Oxygenases - physiology | Von Hippel-Lindau Tumor Suppressor Protein - metabolism | Basic Helix-Loop-Helix Transcription Factors - deficiency | Basic Helix-Loop-Helix Transcription Factors - genetics | Hypoxia-Inducible Factor-Proline Dioxygenases - physiology | Cardiovascular Diseases - metabolism | Hydroxylation | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Hypoxia-Inducible Factor-Proline Dioxygenases - genetics | Hypertension, Pulmonary - metabolism | Cardiovascular System - enzymology | Animals | Iron - physiology | Polycythemia - enzymology | Cardiovascular System - metabolism | Ischemic Preconditioning, Myocardial | Protein Isoforms | Mice | Protein Processing, Post-Translational | Altitude | Hypoxia | oxygen sensing | HIF | 2-oxoglutarate oxygenase | hydroxylase
Journal Article
STEM CELLS, ISSN 1066-5099, 02/2014, Volume 32, Issue 2, pp. 364 - 376
Journal Article
The Journal of Pathology, ISSN 0022-3417, 07/2017, Volume 242, Issue 3, pp. 322 - 333
Osteogenic–angiogenic coupling is promoted by the hypoxia‐inducible factor 1‐alpha (HIF‐1α) transcription factor, provoking interest in HIF activation as a... 
hypoxia‐inducible factor (HIF) | differentiation | PHD2 | osteoclast | bone resorption | hypoxia-inducible factor (HIF) | RHEUMATOID-ARTHRITIS | ACTIVATION | PROLYL HYDROXYLATION | TUMOR | PATHOLOGY | IN-VITRO | ONCOLOGY | H+-ATPASE | NF-KAPPA-B | SKELETAL DEVELOPMENT | Bone Resorption - physiopathology | Osteogenesis - physiology | Humans | RNA, Messenger - metabolism | Hypoxia-Inducible Factor-Proline Dioxygenases - deficiency | Leukocytes, Mononuclear - pathology | Animals | Cell Adhesion - physiology | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Female | Mice | Hypoxia-Inducible Factor 1, alpha Subunit - physiology | Osteoclasts - physiology | Cell Differentiation - physiology | Cancellous Bone - physiology | Prolyl Hydroxylases - physiology | Bone resorption | Bones | Hydroxylases | RNA | Density | Analysis | Osteoprogenitor cells | Hypoxia-inducible factor 1 | Activation | Bone (trabecular) | CD14 antigen | Osteolysis | Osteoblasts | Angiogenesis | Biomedical materials | Hypoxia-inducible factor 1a | Mineralization | Bone marrow | Biocompatibility | Inhibition | Coupling | Hypoxia-inducible factors | Enzymes | Hydroxylase | Gene expression | Diseases | Osteoclastogenesis | Pathology | Monocytes | Bone mass | Glycolysis | Hypoxia | Osteoclasts | Differentiation | Original Papers | Original Paper
Journal Article
Journal Article
Life Sciences, ISSN 0024-3205, 11/2018, Volume 213, pp. 126 - 133
This study investigated the effects of atorvastatin (ATS) on the paraquat (PQ)-induced epithelial-mesenchymal transition (EMT) and the potential mechanism... 
Atorvastatin | Hypoxia-inducible factor | Epithelial-mesenchymal transition | Paraquat | Pulmonary fibrosis | MEDICINE, RESEARCH & EXPERIMENTAL | B16.F10 MELANOMA-CELLS | STATIN USE | ACUTE LUNG INJURY | PPAR-GAMMA RECEPTORS | INDUCED PULMONARY-FIBROSIS | INFLAMMATION | NITRIC-OXIDE | PHARMACOLOGY & PHARMACY | HIF-1-ALPHA | SIMVASTATIN | EXPRESSION | Hypoxia-Inducible Factor 1, alpha Subunit - drug effects | A549 Cells | Cell Line | Cadherins - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Atorvastatin - metabolism | Humans | Rats | Epithelial-Mesenchymal Transition - drug effects | Male | Atorvastatin - pharmacology | Hypoxia-Inducible Factor 1 - metabolism | Rats, Sprague-Dawley | Paraquat - adverse effects | Animals | Signal Transduction - drug effects | Lung Injury - metabolism | Hypoxia | Hypoxia-Inducible Factor 1 - drug effects | Lung - metabolism | Pulmonary Fibrosis - metabolism | Lung Injury - drug therapy | Pulmonary Fibrosis - drug therapy | Zonula Occludens-1 Protein - metabolism | Herbicides | Medical colleges | Respiratory tract diseases | Poisoning | Stem cells | Antilipemic agents | Vimentin | Cell culture | Hypoxia-inducible factor 1 | Mesenchyme | Toxicity | E-cadherin | Hypoxia-inducible factor 1a | Attenuation | Catenin | Statins | Hypoxia-inducible factors | Lung diseases | Markers | Pharmacology | Gene expression | Chemical compounds | Zonula occludens-1 protein | Cell lines | Fibrosis | Index Medicus
Journal Article
Biochemical Journal, ISSN 0264-6021, 04/2013, Volume 451, Issue 2, pp. 185 - 194
H1F1A (hypoxia-inducible factor ice) is the master regulator of the cellular response to hypoxia and is implicated in cancer progression. Whereas the... 
Hypoxia-inducible factor 1a (HIF1A) | AU-rich element (ARE)-mediated degradation (AMD) | Processing body (P-body) | Pseudo-deubiquitinating enzyme (pseudo-DUB) | Poly(A) nuclease 2 (PAN2) | Ubiquitin-specific protease 52 (USP52) | pseudo-deubiquitinating enzyme (pseudo-DUB) | BIOCHEMISTRY & MOLECULAR BIOLOGY | processing body (P-body) | POLY(A)-BINDING PROTEIN | ubiquitin-specific protease 52 (USP52) | GW182 | HYPOXIA | SACCHAROMYCES-CEREVISIAE | INDUCIBLE FACTOR (HIF)-1-ALPHA | DEADENYLASE COMPLEXES | poly(A) nuclease 2 (PAN2) | hypoxia-inducible factor 1 alpha (HIF1A) | BODIES | HIF-1-ALPHA | INDUCED DEGRADATION | POLY(A) NUCLEASE | Proto-Oncogene Proteins - metabolism | Cell Line | Cytoplasmic Structures - genetics | RNA-Binding Proteins - genetics | Exoribonucleases - genetics | Autoantigens - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Humans | Proto-Oncogene Proteins - genetics | RNA Stability | Autoantigens - genetics | AU Rich Elements | Gene Knockdown Techniques | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | 3' Untranslated Regions | Cell Hypoxia - genetics | Exoribonucleases - metabolism | RNA-Binding Proteins - metabolism | Cytoplasmic Structures - metabolism | Poly A | YFP, yellow fluorescent protein | PAN2, poly(A) nuclease 2 | CHX, cycloheximide | DUB, deubiquitinating enzyme | HRE, hypoxia-response element | HEK, human embryonic kidney | RT, reverse transcription | TTP, tristetrapolin | DCP1A, decapping enzyme 1A | UTR, untranslated region | HIF1B, hypoxia-inducible factor 1β | PHD, prolyl hydroxylase | HIF1A, hypoxia-inducible factor 1α | LC, liquid chromatography | siRNA, short interfering RNA | PABPC1, poly(A)-binding protein C1 | TRIM21, tripartite motif-containing 21 | P-body, processing body | USP52, ubiquitin-specific protease 52 | LDHA, lactate dehydrogenase A | GFP, green fluorescent protein | aHIF, antisense hypoxia-inducible factor | VHL, von Hippel–Lindau | FBS, fetal bovine serum | MS, tandem MS | CTNNB1, β-catenin | TCE, transcription elongation factor | VEGF, vascular endothelial growth factor | hypoxia-inducible factor 1α (HIF1A) | CUL2, cullin 2 | AMD, ARE-mediated degradation | miRNA, microRNA | NT, Non-Targeting | FISH, fluorescent in situ hybridization | NEDD8, neural-precursor-cell-expressed developmentally down-regulated 8 | NP-40, Nonidet P40 | ARE, AU-rich element | ERG, Ets-related gene | GLUT1, glucose transporter 1 | CA9, carbonic anhydrase IX
Journal Article
Acta Physiologica, ISSN 1748-1708, 10/2017, Volume 221, Issue 2, pp. 98 - 114
Aim The cardioprotective effects of sevoflurane postconditioning (SpostC) are eliminated under diabetic conditions, and the underlying mechanism for this... 
myocardial protection | deferoxamine | sevoflurane postconditioning | hypoxia‐inducible factor‐1 | diabetes | hypoxia-inducible factor-1 | SURGERY | PHYSIOLOGY | MITOCHONDRIAL | HEARTS | MODEL | ISCHEMIA-REPERFUSION INJURY | IMPROVES | ACCUMULATION | HIF-1-ALPHA | OUTCOMES | EXPRESSION | Anesthetics, Inhalation - pharmacology | Deferoxamine - pharmacology | Up-Regulation | Signal Transduction | Rats | Male | Methyl Ethers - pharmacology | Myocardial Infarction - metabolism | Hypoxia-Inducible Factor 1 - metabolism | Rats, Sprague-Dawley | Siderophores - pharmacology | Hypoxia-Inducible Factor 1 - genetics | Gene Expression Regulation - drug effects | Sevoflurane | Animals | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Ischemic Postconditioning | Myocardial Reperfusion Injury - drug therapy | Diabetes Mellitus, Experimental - metabolism | Heart | Enzymes | Vascular endothelial growth factor | Myocardial infarction | Hypoxia-inducible factor 1 | Reactive oxygen species | Bax protein | Bcl-2 protein | Caspase-3 | Deferoxamine | Proteins | Signal transduction | Mitochondria | Hypoxia-inducible factor 1a | Reperfusion | Ischemia | Ultrastructure | Rodents | Heart diseases | Hypoxia-inducible factors | Diabetes mellitus | Caspase | Myocardium | Hypoxia | Protein expression | Diabetes | Respiration | Electron transport
Journal Article
FEBS Letters, ISSN 0014-5793, 08/2014, Volume 588, Issue 17, pp. 3137 - 3146
Journal Article