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Nature, ISSN 0028-0836, 11/2014, Volume 515, Issue 7527, pp. 431 - 435
Journal Article
Antioxidants & Redox Signaling, ISSN 1523-0864, 10/2011, Volume 15, Issue 7, pp. 1835 - 1846
Journal Article
Biochemical Journal, ISSN 0264-6021, 08/2004, Volume 381, Issue 3, pp. 761 - 767
An important regulator involved in oxygen-dependent gene expression is the transcription factor HIF (hypoxia-inducible factor), which is composed of an... 
Post-translational modification | Hypoxia-inducible factor | Protein degradation | Oxygen sensing | Prolyl hydroxylation | Von-Hippel-Lindau protein | TRANSCRIPTIONAL ACTIVITY | PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | ALPHA | hypoxia-inducible factor | oxygen sensing | post-translational modification | von-Hippel-Lindau protein | FAMILY | OXYGEN | FACTOR-1-ALPHA | GENE-EXPRESSION | HIF-1-ALPHA | VHL | protein degradation | prolyl hydroxylation | Humans | Half-Life | Kidney Neoplasms - metabolism | Ubiquitin-Protein Ligases - physiology | Bone Neoplasms - pathology | Hypoxia-Inducible Factor 1, alpha Subunit | RNA, Messenger - biosynthesis | Liver Neoplasms - pathology | Liver Neoplasms - enzymology | Kidney Tubules, Proximal - cytology | DNA-Binding Proteins - physiology | Hypoxia - enzymology | Hydroxylation | Hypoxia-Inducible Factor 1 | Immediate-Early Proteins - biosynthesis | Carcinoma, Hepatocellular - enzymology | Tumor Suppressor Proteins - physiology | Epithelial Cells - enzymology | Liver Neoplasms - metabolism | Cell Line, Tumor | Von Hippel-Lindau Tumor Suppressor Protein | Enzyme Induction - physiology | Osteosarcoma - pathology | Carcinoma, Hepatocellular - metabolism | Epithelial Cells - metabolism | Gene Expression Regulation, Enzymologic - physiology | Oxygen - metabolism | Procollagen-Proline Dioxygenase - biosynthesis | Bone Neoplasms - metabolism | Procollagen-Proline Dioxygenase - metabolism | DNA-Binding Proteins - metabolism | Kidney Tubules, Proximal - enzymology | Gene Expression Regulation, Neoplastic - physiology | Osteosarcoma - metabolism | Cell Line | Transcription Factors - physiology | Bone Neoplasms - enzymology | Osteosarcoma - enzymology | Adenocarcinoma, Clear Cell - metabolism | Nuclear Proteins - metabolism | Hypoxia-Inducible Factor-Proline Dioxygenases | Dioxygenases | Transcription Factors - metabolism | Kidney Neoplasms - enzymology | Carcinoma, Hepatocellular - pathology | Kidney Tubules, Proximal - metabolism | Kidney Neoplasms - pathology | Adenocarcinoma, Clear Cell - pathology | Nuclear Proteins - physiology | Adenocarcinoma, Clear Cell - enzymology | DNA-Binding Proteins - biosynthesis | ODD, oxygen-dependent degradation domain | aRP, acidic ribosomal protein | RNAi, RNA interference | pVHL, von-Hippel-Lindau protein | EGLN, egg-laying deficient nine-like protein | HIF, hypoxia-inducible factor | siRNA, small interfering RNA | IVTT, in vitro transcription | PHD, prolyl hydroxylase domain containing protein | translation | RT, reverse transcriptase | RPTEC, human renal proximal tubular epithelial cells
Journal Article
Circulation Research, ISSN 0009-7330, 08/2007, Volume 101, Issue 3, pp. 258 - 267
Nonphagocytic NADPH oxidases have recently been suggested to play a major role in the regulation of physiological and pathophysiological processes, in... 
Vascular smooth muscle cell proliferation | Hypoxia | Hypoxic pulmonary vasoconstriction | NADPH oxidase | Pulmonary hypertension | hypoxia | CARDIAC & CARDIOVASCULAR SYSTEMS | TGF-BETA | hypoxic pulmonary vasoconstriction | SUPEROXIDE-PRODUCTION | pulmonary hypertension | PROLIFERATION | vascular smooth muscle cell proliferation | NAD(P)H OXIDASE | ENDOTHELIAL-CELLS | GENE-EXPRESSION | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | CARDIOVASCULAR-DISEASES | ARTERY | HEMATOLOGY | VASOCONSTRICTION | Membrane Glycoproteins - analysis | Oxygen - pharmacology | Protein Subunits | Tunica Media - pathology | Humans | Myocytes, Smooth Muscle - pathology | Hypertension, Pulmonary - physiopathology | Male | Oxygen - metabolism | RNA, Messenger - biosynthesis | RNA Interference | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Cell Division | Drug Design | Superoxides - metabolism | NADPH Oxidases - genetics | Female | Hypertension, Pulmonary - drug therapy | NADPH Oxidases - biosynthesis | Hypertension, Pulmonary - enzymology | Endoplasmic Reticulum - enzymology | Cells, Cultured - drug effects | Hypoxia - enzymology | Myocytes, Smooth Muscle - enzymology | NADPH Oxidases - analysis | RNA, Small Interfering - pharmacology | Enzyme Induction | Nitric Oxide - physiology | Hypoxia - complications | NADPH Oxidase 4 | Organ Specificity | NADPH Oxidase 2 | Transforming Growth Factor beta1 - physiology | Cells, Cultured - enzymology | Pulmonary Artery - enzymology | Pulmonary Artery - cytology | Animals | Hypoxia - physiopathology | Lung - blood supply | Chronic Disease | Hypertension, Pulmonary - etiology | NADPH Oxidases - physiology | Tunica Media - enzymology | Hypertrophy
Journal Article
Journal Article
by Mao, M and Zhang, M and Ge, AQ and Ge, X and Gu, R and Zhang, C and Fu, Y and Gao, JY and Wang, XY and Liu, Y and Zhu, DL
CELL DEATH & DISEASE, ISSN 2041-4889, 02/2018, Volume 9, Issue 2, pp. 221 - 10
Calcification is a major risk factor for vascular integrity. This pathological symptom and the underlying mechanisms in hypoxic pulmonary artery hypertension... 
APOPTOSIS | STIM1 | CHAPERONE-MEDIATED AUTOPHAGY | INFLAMMATION | ARTERIAL-HYPERTENSION | DISEASE | DEGRADATION | MECHANISMS | 15-LIPOXYGENASE | EXPRESSION | CELL BIOLOGY | Calcinosis - genetics | Rats, Wistar | Myocytes, Smooth Muscle - pathology | Apoptosis - genetics | Male | Killer Cells, Natural - pathology | Granzymes - genetics | Calcinosis - chemically induced | Hypertension, Pulmonary - chemically induced | T-Lymphocytes, Cytotoxic - pathology | Cell Differentiation | Hypertension, Pulmonary - enzymology | Monocrotaline - administration & dosage | Hypoxia - enzymology | Calcium Channels | Osteoblasts - enzymology | Signal Transduction | Myocytes, Smooth Muscle - enzymology | Mice, Inbred C57BL | Gene Expression Regulation | Hypertension, Pulmonary - genetics | Mice, Transgenic | Calcinosis - enzymology | Rats, Sprague-Dawley | T-Lymphocytes, Cytotoxic - enzymology | Pulmonary Artery - enzymology | Killer Cells, Natural - enzymology | Granzymes - deficiency | Osteoblasts - pathology | Hypoxia - genetics | Muscle, Smooth, Vascular - pathology | Animals | Hypoxia - pathology | Mice | Hypoxia - chemically induced | Primary Cell Culture | Calcinosis - pathology | Hypertension, Pulmonary - pathology | Muscle, Smooth, Vascular - enzymology | Pulmonary Artery - pathology | Hypertension | Calcification (ectopic) | Phenotypes | Calcium channels | Animal models | Pulmonary arteries | Cytotoxicity | Smooth muscle | Lymphocytes T | Osteoblasts | Pulmonary artery | Granzyme B | Osteoblastogenesis | Mineralization | Arteriosclerosis | Calcification | Hypoxia | Natural killer cells | Apoptosis
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 07/2014, Volume 34, Issue 7, pp. 1446 - 1458
OBJECTIVE—Pulmonary vascular remodeling, the pathological hallmark of pulmonary arterial hypertension, is attributed to proliferation, apoptosis resistance,... 
anoxia | muscle | pulmonary | protein-lysine 6-oxidase | hypertension | extracellular matrix | smooth | COLLAGEN | muscle, smooth | AORTIC-ANEURYSMS | RAT | BONE MORPHOGENETIC PROTEIN | hypertension, pulmonary | PROLIFERATION | HYPOXIA | CROSS-TALK | GROWTH-FACTORS | ELASTIN | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | HEMATOLOGY | Antihypertensive Agents - pharmacology | Fibroblasts - enzymology | Humans | Middle Aged | Monocrotaline | Myocytes, Smooth Muscle - pathology | Male | Hypertrophy, Right Ventricular - etiology | RNA, Messenger - metabolism | Ventricular Dysfunction, Right - enzymology | Case-Control Studies | Cell Hypoxia | Young Adult | Aged, 80 and over | Adult | Female | Ventricular Dysfunction, Right - physiopathology | Hypertension, Pulmonary - drug therapy | Hypertension, Pulmonary - enzymology | Disease Models, Animal | Elastin - metabolism | Isoenzymes | Myocytes, Smooth Muscle - enzymology | Cells, Cultured | Enzyme Inhibitors - pharmacology | Rats | Familial Primary Pulmonary Hypertension | Hypertension, Pulmonary - genetics | Hypoxia - complications | Pulmonary Artery - drug effects | Fibroblasts - pathology | Hypertrophy, Right Ventricular - enzymology | Pulmonary Artery - enzymology | Gene Expression Regulation, Enzymologic | Ventricular Dysfunction, Right - prevention & control | Collagen - metabolism | Protein-Lysine 6-Oxidase - antagonists & inhibitors | Muscle, Smooth, Vascular - pathology | Animals | Ventricular Dysfunction, Right - etiology | Protein-Lysine 6-Oxidase - metabolism | Hypertrophy, Right Ventricular - prevention & control | Mice | Protein-Lysine 6-Oxidase - genetics | Hypertension, Pulmonary - etiology | Hypertension, Pulmonary - pathology | Muscle, Smooth, Vascular - enzymology | Pulmonary Artery - pathology
Journal Article
The Journal of Immunology, ISSN 0022-1767, 06/2007, Volume 178, Issue 11, pp. 7405 - 7411
Journal Article
Circulation Research, ISSN 0009-7330, 05/2012, Volume 110, Issue 11, pp. 1423 - 1434
RATIONALE:RhoA and Rho kinase contribute to pulmonary vasoconstriction and vascular remodeling in pulmonary hypertension. RhoB, a protein homologous to RhoA... 
smooth muscle cells | endothelium | hypoxia | Rho GTPases | pulmonary hypertension | TRANSFORMATION | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | KINASE INHIBITORS | NEURAL CREST CELLS | FARNESYLTRANSFERASE INHIBITORS | RAC | EPIDERMAL-GROWTH-FACTOR | PERIPHERAL VASCULAR DISEASE | MICE | ACTIN CYTOSKELETON | HYPERTENSION | HEMATOLOGY | Cell Proliferation | Humans | Male | rhoA GTP-Binding Protein - metabolism | rhoB GTP-Binding Protein - metabolism | Actomyosin - genetics | RNA Interference | Time Factors | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Farnesyltranstransferase - antagonists & inhibitors | Hypertension, Pulmonary - drug therapy | rhoB GTP-Binding Protein - genetics | Myocytes, Smooth Muscle - drug effects | Hypertension, Pulmonary - enzymology | Disease Models, Animal | Muscle, Smooth, Vascular - drug effects | Hypoxia - enzymology | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Myocytes, Smooth Muscle - enzymology | Polyenes - pharmacology | Stress Fibers - enzymology | Enzyme Inhibitors - pharmacology | Familial Primary Pulmonary Hypertension | Hypoxia - complications | Actomyosin - metabolism | Pulmonary Artery - enzymology | Mice, Knockout | Polyunsaturated Alkamides - pharmacology | Mice | Myosin Light Chains - metabolism | Enzyme Activation | Chronic Disease | Endothelial Cells - enzymology | Hypertension, Pulmonary - etiology | Muscle, Smooth, Vascular - enzymology | Cell Movement | Phosphorylation | Capillary Permeability | Serine | Cell Hypoxia | Farnesyltranstransferase - metabolism | Transfection | Mice, Inbred C57BL | Cells, Cultured | Vasoconstriction | Hypertension, Pulmonary - genetics | Hypoxia - genetics | Animals | rhoB GTP-Binding Protein - deficiency | Endothelial Cells - drug effects | Medical and Health Sciences | Medicin och hälsovetenskap
Journal Article
Circulation Research, ISSN 0009-7330, 05/2012, Volume 110, Issue 11, pp. 1484 - 1497
RATIONALE:Pulmonary arterial hypertension (PAH) is a lethal syndrome characterized by pulmonary vascular obstruction caused, in part, by pulmonary artery... 
mitotic checkpoint | cyclin B1/cyclin-dependent kinase 1 | mitochondrial fission | hypoxia-inducible factor-1 | mitochondrial division inhibitor-1 | CARDIAC & CARDIOVASCULAR SYSTEMS | ENTRY | INDUCIBLE FACTOR 1-ALPHA | HYPOXIA | DRP1 | PATHWAY | ARTERIAL-HYPERTENSION | ENDOTHELIAL-CELLS | GENE-EXPRESSION | GERMLINE MUTATIONS | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | K+ CHANNELS | Antihypertensive Agents - pharmacology | Humans | Monocrotaline | Male | Cyclin B1 - metabolism | Cobalt | Hypertension, Pulmonary - therapy | CDC2 Protein Kinase - metabolism | RNA Interference | Time Factors | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Mitochondrial Proteins - metabolism | Myocytes, Smooth Muscle - drug effects | Hypertension, Pulmonary - enzymology | Disease Models, Animal | Muscle, Smooth, Vascular - drug effects | Myocytes, Smooth Muscle - enzymology | Dynamins - genetics | Rats | Familial Primary Pulmonary Hypertension | Hypoxia - complications | Rats, Sprague-Dawley | Pulmonary Artery - enzymology | Cell Cycle Checkpoints | GTP Phosphohydrolases - metabolism | GTP Phosphohydrolases - genetics | Mitochondria, Muscle - drug effects | Enzyme Activation | Hypertension, Pulmonary - etiology | Muscle, Smooth, Vascular - enzymology | Dynamins - metabolism | Phosphorylation | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Serine | Myocytes, Smooth Muscle - pathology | Mitochondrial Proteins - genetics | Case-Control Studies | Transfection | Quinazolinones - pharmacology | Mitochondria, Muscle - enzymology | Mitochondria, Muscle - pathology | Cells, Cultured | Muscle, Smooth, Vascular - pathology | Animals | Mitosis - drug effects | Glycolysis | Cell Proliferation - drug effects | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology | Genetic Therapy - methods | Hypoxia-inducible factor 1 | CDK1-cyclin B1 | Mitochondrial division inhibitor-1 (Mdivi-1) | Mitochondrial fission | Mitotic check point
Journal Article
Journal Article
Journal Article
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