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1. Full Text Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS
by Chouchani, Edward T and Pell, Victoria R and Gaude, Edoardo and Aksentijević, Dunja and Sundier, Stephanie Y and Robb, Ellen L and Logan, Angela and Nadtochiy, Sergiy M and Ord, Emily N. J and Smith, Anthony C and Eyassu, Filmon and Shirley, Rachel and Hu, Chou-Hui and Dare, Anna J and James, Andrew M and Rogatti, Sebastian and Hartley, Richard C and Eaton, Simon and Costa, Ana S. H and Brookes, Paul S and Davidson, Sean M and Duchen, Michael R and Saeb-Parsy, Kourosh and Shattock, Michael J and Robinson, Alan J and Work, Lorraine M and Frezza, Christian and Krieg, Thomas and Murphy, Michael P
Nature, ISSN 0028-0836, 11/2014, Volume 515, Issue 7527, pp. 431 - 435
Ischaemia-reperfusion injury occurs when the blood supply to an organ is disrupted and then restored, and underlies many disorders, notably heart attack and... 
STROKE | HYPOXIA-ISCHEMIA | MECHANISM | COMPLEX-I | SUPEROXIDE-PRODUCTION | MULTIDISCIPLINARY SCIENCES | PURINE NUCLEOTIDE CYCLE | CONSEQUENCES | CARDIOPROTECTION | HYPERTENSIVE-RATS | DEHYDROGENASE | Metabolomics | Mitochondria - enzymology | Electron Transport | Reactive Oxygen Species - metabolism | Ischemia - enzymology | Male | Electron Transport Complex I - metabolism | Myocytes, Cardiac - enzymology | Myocardium - metabolism | Malates - metabolism | Reperfusion Injury - metabolism | NAD - metabolism | Disease Models, Animal | Myocardial Infarction - enzymology | Adenosine Monophosphate - metabolism | Reperfusion Injury - enzymology | Ischemia - metabolism | Mitochondria - metabolism | Myocardial Infarction - metabolism | Citric Acid Cycle | Myocardium - cytology | Stroke - enzymology | Myocardium - enzymology | Stroke - metabolism | Animals | Succinic Acid - metabolism | Fumarates - metabolism | Myocytes, Cardiac - metabolism | Aspartic Acid - metabolism | Succinate Dehydrogenase - metabolism | Mice | Reactive oxygen species | Research | Succinates | Health aspects | Analysis | Reperfusion injury | Heart | Stroke | Glucose | Metabolites | Metabolism | Carbon
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2. Full Text A Central Role of Heme Oxygenase-1 in Cardiovascular Protection
by Wu, Meng-Ling and Ho, Yen-Chun and Yet, Shaw-Fang
Antioxidants & Redox Signaling, ISSN 1523-0864, 10/2011, Volume 15, Issue 7, pp. 1835 - 1846
The intrinsic defense mechanisms of the body are critical in protecting tissues from injury in response to pathological stress. Heme oxygenase-1 (HO-1), a... 
Forum Review Articles | GRAFT ARTERIOSCLEROSIS | ENDOTHELIAL PROGENITOR CELLS | MATRIX METALLOPROTEINASES | CARBON-MONOXIDE | BIOCHEMISTRY & MOLECULAR BIOLOGY | ENDOCRINOLOGY & METABOLISM | ACUTE MYOCARDIAL-INFARCTION | ATHEROSCLEROTIC LESION FORMATION | SMOOTH-MUSCLE-CELLS | CORONARY-ARTERY-DISEASE | SIROLIMUS-ELUTING STENTS | MICROSATELLITE POLYMORPHISM | Genetic Therapy | Heme Oxygenase-1 - metabolism | Diabetes Complications | Humans | Arteries - injuries | Heme Oxygenase-1 - genetics | Neovascularization, Pathologic - enzymology | Atherosclerosis - enzymology | Plaque, Atherosclerotic - enzymology | Plaque, Atherosclerotic - pathology | Graft Rejection - pathology | Microsatellite Repeats | Graft Rejection - enzymology | Atherosclerosis - pathology | Coronary Vessels - pathology | Coronary Vessels - enzymology | Thrombosis - enzymology | Myocardium - pathology | Graft Occlusion, Vascular - enzymology | Heart Diseases - enzymology | Thrombosis - pathology | Heart Diseases - etiology | Myocardium - enzymology | Animals | Arteries - enzymology | Graft Occlusion, Vascular - pathology | Heart Diseases - therapy | Hypoxia | Heart Diseases - pathology | Oxidases | Physiological aspects | Care and treatment | Research | Cardiovascular diseases
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3. Full Text Hypoxia-inducible factor-1 (HIF-1) promotes its degradation by induction of HIF-α-prolyl-4-hydroxylases
by Marxsen, Jan H and Stengel, Petra and Doege, Kathrin and Heikkinen, Pekka and Jokilehto, Terhi and Wagner, Thomas and Jelkmann, Wolfgang and Jaakkola, Panu and Metzen, Eric
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
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4. Full Text Hypoxia-Dependent Regulation of Nonphagocytic NADPH Oxidase Subunit NOX4 in the Pulmonary Vasculature
by Mittal, Manish and Roth, Markus and König, Peter and Hofmann, Simone and Dony, Eva and Goyal, Parag and Selbitz, Anne-Christin and Schermuly, Ralph Theo and Ghofrani, Hossein Ardeschir and Kwapiszewska, Grazyna and Kummer, Wolfgang and Klepetko, Walter and Hoda, Mir Ali Reza and Fink, Ludger and Hänze, Jörg and Seeger, Werner and Grimminger, Friedrich and Schmidt, Harald H.H.W and Weissmann, Norbert
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
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5. Full Text A Feedback Loop Involving the Phd3 Prolyl Hydroxylase Tunes the Mammalian Hypoxic Response In Vivo
by Yoji Andrew Minamishima and Javid Moslehi and Robert F. Padera and Roderick T. Bronson and Ronglih Liao and William G. Kaelin Jr
Molecular and Cellular Biology, ISSN 0270-7306, 11/2009, Volume 29, Issue 21, pp. 5729 - 5741
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... 
INACTIVATION | HEART | TRANSCRIPTIONAL ACTIVITY | MYOCARDIAL-INFARCTION | HIF | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOCHONDRIAL AUTOPHAGY | MOUSE MODEL | VASCULAR TUMORS | INDUCIBLE-FACTOR | PAS DOMAIN PROTEIN | CELL BIOLOGY | Mitochondria - enzymology | Liver - pathology | Liver - enzymology | Kidney - pathology | Kidney - enzymology | Polycythemia - complications | Cardiomyopathies - enzymology | Procollagen-Proline Dioxygenase - metabolism | Cell Hypoxia | Cardiomyopathies - physiopathology | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Heart Function Tests | Von Hippel-Lindau Tumor Suppressor Protein - metabolism | Myocardium - ultrastructure | Mammals - metabolism | Cardiomegaly - physiopathology | Hypoxia-Inducible Factor-Proline Dioxygenases | Cardiomegaly - enzymology | Mitochondria - pathology | Cardiomegaly - complications | Feedback, Physiological | Myocardium - enzymology | Animals | Polycythemia - enzymology | Procollagen-Proline Dioxygenase - deficiency | Survival Analysis | Cardiomyopathies - complications | Mice | Polycythemia - physiopathology | Enzyme Activation
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6. Full Text Granzyme B deficiency promotes osteoblastic differentiation and calcification of vascular smooth muscle cells in hypoxic pulmonary hypertension
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
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7. Full Text Lysyl Oxidases Play a Causal Role in Vascular Remodeling in Clinical and Experimental Pulmonary Arterial Hypertension
by Nave, Alexander H and Mižíková, Ivana and Niess, Gero and Steenbock, Heiko and Reichenberger, Frank and Talavera, María L and Veit, Florian and Herold, Susanne and Mayer, Konstantin and Vadász, István and Weissmann, Norbert and Seeger, Werner and Brinckmann, Jürgen and Morty, Rory E
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
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8. Full Text Expression of Tie-2 by Human Monocytes and Their Responses to Angiopoietin-2
by Murdoch, Craig and Tazzyman, Simon and Webster, Steve and Lewis, Claire E
The Journal of Immunology, ISSN 0022-1767, 06/2007, Volume 178, Issue 11, pp. 7405 - 7411
Angiopoietins 1 and 2 bind to Tie-2 expressed on endothelial cells and regulate vessel stabilization and angiogenesis. Tie-2(+) monocytes have been shown to be... 
TUMOR-NECROSIS-FACTOR | HUMAN PERIPHERAL-BLOOD | ANGIOGENESIS | MACROPHAGES | INFLAMMATION | ENDOTHELIAL-CELLS | IN-VIVO | VESSEL FORMATION | RECEPTOR | IMMUNOLOGY | HYPOXIA | Cell Hypoxia - immunology | Humans | Neoplasms, Experimental - enzymology | Monocytes - metabolism | Neoplasms, Experimental - pathology | Lymphocyte Subsets - metabolism | RNA, Messenger - biosynthesis | Cell Membrane - pathology | Monocytes - pathology | Angiopoietin-2 - physiology | Granulocytes - pathology | Neovascularization, Pathologic - immunology | Granulocytes - metabolism | Receptor, TIE-2 - physiology | Inflammation Mediators - physiology | Lymphocyte Subsets - pathology | Cytokines - metabolism | Macrophages - pathology | Gene Expression Regulation - immunology | RNA, Messenger - genetics | Receptor, TIE-2 - biosynthesis | Cells, Cultured | Granulocytes - enzymology | Macrophages - enzymology | Receptor, TIE-2 - genetics | Cell Membrane - enzymology | Monocytes - enzymology | Macrophages - metabolism | Animals | Up-Regulation - immunology | Lymphocyte Subsets - enzymology | Cell Membrane - immunology | Mice | Cytokines - antagonists & inhibitors | Chemotaxis, Leukocyte - immunology | Neoplasms, Experimental - blood supply
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9. Full Text Role of RhoB in the Regulation of Pulmonary Endothelial and Smooth Muscle Cell Responses to Hypoxia
by Wojciak-Stothard, Beata and Zhao, Lan and Oliver, Eduardo and Dubois, Olivier and Wu, Yixing and Kardassis, Dimitris and Vasilaki, Eleftheria and Huang, Minzhou and Mitchell, Jane A and Harrington, Louise S and Prendergast, George C and Wilkins, Martin R and Medicinska och farmaceutiska vetenskapsområdet and Uppsala universitet and Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm and Ludwiginstitutet för cancerforskning
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
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10. Full Text Dynamin-Related Protein 1–Mediated Mitochondrial Mitotic Fission Permits Hyperproliferation of Vascular Smooth Muscle Cells and Offers a Novel Therapeutic Target in Pulmonary Hypertension
by Marsboom, Glenn and Toth, Peter T and Ryan, John J and Hong, Zhigang and Wu, Xichen and Fang, Yong-Hu and Thenappan, Thenappan and Piao, Lin and Zhang, Hannah J and Pogoriler, Jennifer and Chen, Yimei and Morrow, Erik and Weir, E Kenneth and Rehman, Jalees and Archer, Stephen L
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
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11. Full Text A Catalytic Role for Proangiogenic Marrow-Derived Cells in Tumor Neovascularization
by Seandel, Marco and Butler, Jason and Lyden, David and Rafii, Shahin
Cancer Cell, ISSN 1535-6108, 2008, Volume 13, Issue 3, pp. 181 - 183
Small numbers of proangiogenic bone marrow-derived cells (BMDCs) can play pivotal roles in tumor progression. In this issue of , two papers, utilizing... 
RECRUITMENT | COLLAGEN | ANGIOGENESIS | ONCOLOGY | GROWTH | RELEASE | MMP-9 | Myeloid Cells - enzymology | Glioblastoma - enzymology | Bone Marrow Cells - enzymology | Neoplasms, Experimental - enzymology | Hypoxia-Inducible Factor 1, alpha Subunit - deficiency | Neovascularization, Pathologic - pathology | Cell Hypoxia | Neoplasms, Experimental - pathology | Neovascularization, Pathologic - enzymology | Matrix Metalloproteinase 9 - metabolism | Monocytes - transplantation | Stem Cells - enzymology | Time Factors | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Matrix Metalloproteinase 9 - genetics | Bone Marrow Transplantation | Neovascularization, Pathologic - prevention & control | Signal Transduction | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Neoplasm Invasiveness | Neoplasms, Experimental - therapy | Matrix Metalloproteinase 9 - deficiency | Mice, Knockout | Monocytes - enzymology | Animals | Myeloid Cells - transplantation | Mice | Angiogenic Proteins - metabolism | Endothelial Cells - enzymology | Glioblastoma - blood supply | Cell Movement | Neoplasms, Experimental - blood supply | Development and progression | Neovascularization | Analysis | Tumors
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12. Full Text HDAC4 Regulates Neuronal Survival in Normal and Diseased Retinas
by Bo Chen and Constance L. Cepko
Science, ISSN 0036-8075, 1/2009, Volume 323, Issue 5911, pp. 256 - 259
Histone deacetylase 4 (HDAC4) shuttles between the nucleus and cytoplasm and serves as a nuclear co-repressor that regulates bone and muscle development. We... 
Retinal rods | Neurons | Neuroglia | Stem cells | Amacrine cells | Retinal degeneration | Photoreceptors | Retina | Reports | Physiological regulation | Cytoplasm | CONTROLS CHONDROCYTE HYPERTROPHY | MULTIDISCIPLINARY SCIENCES | MOUSE | MEF2 TRANSCRIPTION FACTOR | PHOSPHODIESTERASE | DIFFERENTIATION | RETINITIS-PIGMENTOSA | BETA-SUBUNIT | INTRACELLULAR TRAFFICKING | CELL-DEATH | DEGENERATION | Cytoplasm - enzymology | Histone Deacetylases - genetics | Cell Survival | Electroporation | Histone Deacetylases - metabolism | Rhodopsin - metabolism | Cell Nucleus - enzymology | Animals | Rhodopsin - genetics | Transfection | Retina - cytology | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Retina - enzymology | Retinal Rod Photoreceptor Cells - physiology | Retinal Rod Photoreceptor Cells - enzymology | Mice | Acetylation | Mutation | Retinal Degeneration - pathology | Retinal Neurons - enzymology | Retinal Degeneration - enzymology | Retinal Neurons - physiology | Apoptosis | Histones | Cell physiology | Research | Properties | Genetics | Neurosciences | Ophthalmology | Rodents
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13.