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The Journal of Immunology, ISSN 0022-1767, 01/2004, Volume 172, Issue 1, pp. 567 - 576
The signaling mechanism by which the anti-inflammatory cytokine IL-10 mediates suppression of proinflammatory cytokine synthesis remains largely unknown.... 
RHEUMATOID-ARTHRITIS | TUMOR-NECROSIS-FACTOR | DNA-BINDING | HUMAN NEUTROPHILS | TYROSINE PHOSPHORYLATION | INTERLEUKIN-10 RECEPTOR | GENE-EXPRESSION | KAPPA-B-ALPHA | IMMUNOLOGY | HUMAN MONOCYTES | MONONUCLEAR PHAGOCYTES | Protein Binding - genetics | Protein Biosynthesis | Interleukin-6 - antagonists & inhibitors | Humans | Tumor Necrosis Factor-alpha - genetics | Immunoglobulins - genetics | Lipopolysaccharides - antagonists & inhibitors | RNA, Messenger - metabolism | Suppressor of Cytokine Signaling Proteins | Repressor Proteins - antagonists & inhibitors | Antigens, CD - metabolism | Trans-Activators - physiology | Protein Tyrosine Phosphatases - antagonists & inhibitors | RNA, Messenger - biosynthesis | Protein Tyrosine Phosphatases - genetics | Inflammation Mediators - physiology | Glycoproteins - genetics | DNA-Binding Proteins - physiology | Protein Tyrosine Phosphatases - biosynthesis | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction - genetics | DNA - metabolism | Down-Regulation - genetics | Macrophages - metabolism | Protein Tyrosine Phosphatase, Non-Receptor Type 2 | Repressor Proteins - biosynthesis | Up-Regulation - immunology | Interleukin-10 - antagonists & inhibitors | Lipopolysaccharides - pharmacology | Adenoviruses, Human - genetics | Interleukin-10 - immunology | Tumor Necrosis Factor-alpha - biosynthesis | Phosphorylation | Tissue Inhibitor of Metalloproteinase-1 - biosynthesis | Antigens, CD - biosynthesis | Receptors, Cell Surface | Receptors, IgG - biosynthesis | Receptors, IgG - antagonists & inhibitors | Interleukin-10 - physiology | Signal Transduction - immunology | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Signaling Lymphocytic Activation Molecule Family Member 1 | Receptors, Tumor Necrosis Factor - antagonists & inhibitors | RNA, Messenger - antagonists & inhibitors | Receptors, Tumor Necrosis Factor, Type II | Trans-Activators - genetics | Inflammation Mediators - antagonists & inhibitors | Trans-Activators - biosynthesis | Immunoglobulins - biosynthesis | Macrophages - immunology | Inflammation Mediators - immunology | Receptors, Tumor Necrosis Factor - metabolism | Immune Sera - pharmacology | Proteins - physiology | Cells, Cultured | Glycoproteins - antagonists & inhibitors | Histocompatibility Antigens Class II - biosynthesis | Tissue Inhibitor of Metalloproteinase-1 - antagonists & inhibitors | Transcription Factors - antagonists & inhibitors | Transcription Factors - biosynthesis | Up-Regulation - genetics | DNA-Binding Proteins - genetics | DNA - antagonists & inhibitors | Glycoproteins - biosynthesis | Suppressor of Cytokine Signaling 3 Protein | Down-Regulation - immunology | Interleukin-6 - biosynthesis | Receptors, Tumor Necrosis Factor - biosynthesis | STAT3 Transcription Factor | Trans-Activators - antagonists & inhibitors | Genetic Vectors | DNA-Binding Proteins - biosynthesis | Tumor Necrosis Factor-alpha - antagonists & inhibitors | SOCS-3 protein | Index Medicus | Abridged Index Medicus
Journal Article
Immunity, ISSN 1074-7613, 04/2014, Volume 40, Issue 4, pp. 477 - 489
We identified three retinoid-related orphan receptor gamma t (RORγt)-specific inhibitors that suppress T helper 17 (Th17) cell responses, including... 
PATHWAYS | TARGET GENES | FOXP3 OCCUPANCY | T(H)17 | REGULATORY NETWORK | RECEPTOR | DIFFERENTIATION | IMMUNOLOGY | PSORIASIS | ANTI-INTERLEUKIN-17 MONOCLONAL-ANTIBODY | TH17 CELLS | Myelin-Oligodendrocyte Glycoprotein - immunology | T-Lymphocyte Subsets - immunology | Transcription, Genetic - drug effects | Nuclear Receptor Subfamily 1, Group F, Member 3 - antagonists & inhibitors | Humans | Transcriptional Activation - drug effects | Encephalomyelitis, Autoimmune, Experimental - immunology | Structure-Activity Relationship | Gene Regulatory Networks - drug effects | Cell Lineage - drug effects | Systems Biology | Benzhydryl Compounds - chemistry | Heterocyclic Compounds, 4 or More Rings - pharmacology | Th17 Cells - drug effects | T-Lymphocyte Subsets - drug effects | Peptide Fragments - immunology | Protein Binding - drug effects | Benzeneacetamides - chemistry | Benzeneacetamides - pharmacology | Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics | Cytokines - metabolism | Encephalomyelitis, Autoimmune, Experimental - drug therapy | Mice, Inbred C57BL | Heterocyclic Compounds, 4 or More Rings - chemistry | Digoxin - chemistry | Digoxin - pharmacology | Mice, Knockout | Animals | Androstenols - chemistry | Cell Differentiation - drug effects | Cell Line, Tumor | Multiple Sclerosis - immunology | Th17 Cells - immunology | Benzhydryl Compounds - pharmacology | Mice | Multiple Sclerosis - drug therapy | Index Medicus
Journal Article
Diabetes, ISSN 0012-1797, 11/2012, Volume 61, Issue 11, pp. 2842 - 2850
In insulin-secreting cells, expression of NADPH oxidase (NOX), a potent source of ROS, has been reported, along with controversial findings regarding its... 
SIGNAL-TRANSDUCTION | NAD(P)H OXIDASE | RESPIRATORY BURST | OXIDATIVE STRESS | PROTEIN | ISLETS | SUPEROXIDE-PRODUCTION | ENDOTHELIAL-CELLS | ENDOCRINOLOGY & METABOLISM | PANCREATIC BETA-CELLS | DEPENDENT PATHWAY | Islets of Langerhans - drug effects | Reactive Oxygen Species - metabolism | Membrane Glycoproteins - metabolism | Humans | NADPH Oxidases - metabolism | Secretory Vesicles - metabolism | Insulin-Secreting Cells - metabolism | Membrane Glycoproteins - antagonists & inhibitors | Islets of Langerhans - metabolism | Isoenzymes - metabolism | Islets of Langerhans - cytology | NADPH Oxidases - genetics | Insulin-Secreting Cells - cytology | Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors | Cyclic AMP - metabolism | Insulin Secretion | Cyclic AMP-Dependent Protein Kinases - metabolism | Second Messenger Systems - drug effects | Glucagon-Like Peptide 1 - metabolism | Isoenzymes - genetics | Tissue Culture Techniques | Mice, Inbred C57BL | NADPH Oxidases - antagonists & inhibitors | Cells, Cultured | Gene Silencing | NADPH Oxidase 2 | Membrane Glycoproteins - genetics | Mice, Knockout | Cyclic AMP - antagonists & inhibitors | Insulin - metabolism | Animals | Insulin-Secreting Cells - drug effects | Secretory Vesicles - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | RNA, Small Interfering | Cyclic AMP - agonists | Isoenzymes - antagonists & inhibitors | Oxidases | Physiological aspects | Pancreatic beta cells | Research | Analysis | NADP (Coenzyme) | Index Medicus | Abridged Index Medicus | Islet Studies
Journal Article
Cancer Discovery, ISSN 2159-8274, 04/2017, Volume 7, Issue 4, pp. 400 - 409
Entrectinib, a potent oral inhibitor of the tyrosine kinases TRKA/B/C, ROS1, and ALK, was evaluated in two phase I studies in patients with advanced or... 
REARRANGEMENT | ONCOGENE | ONCOLOGY | ANALOG SECRETORY CARCINOMA | LANDSCAPE | KINASE FUSIONS | SARCOMAS | ETV6-NTRK3 GENE FUSION | CRIZOTINIB | GENOMIC ALTERATIONS | CLINICAL-RESPONSE | Benzamides - pharmacokinetics | Colorectal Neoplasms - genetics | Humans | Middle Aged | Receptor, trkA - antagonists & inhibitors | Male | Receptor, trkB - genetics | Indazoles - administration & dosage | Protein Kinase Inhibitors - adverse effects | Mammary Analogue Secretory Carcinoma - genetics | Dose-Response Relationship, Drug | Benzamides - administration & dosage | Membrane Glycoproteins - antagonists & inhibitors | Receptor, trkC - genetics | Anaplastic Lymphoma Kinase | Melanoma - genetics | Colorectal Neoplasms - drug therapy | Receptor, trkB - antagonists & inhibitors | Aged, 80 and over | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Adult | Female | Benzamides - adverse effects | Carcinoma, Non-Small-Cell Lung - pathology | Crizotinib | Protein Kinase Inhibitors - pharmacokinetics | Proto-Oncogene Proteins - antagonists & inhibitors | Pyridines - administration & dosage | Carcinoma, Non-Small-Cell Lung - genetics | Receptor, trkC - antagonists & inhibitors | Melanoma - pathology | Mammary Analogue Secretory Carcinoma - drug therapy | Membrane Glycoproteins - genetics | Protein Kinase Inhibitors - administration & dosage | Sequestosome-1 Protein - genetics | Pyrazoles - administration & dosage | Indazoles - pharmacokinetics | Receptor Protein-Tyrosine Kinases - genetics | Oncogene Proteins, Fusion - genetics | Melanoma - drug therapy | Adolescent | Receptor, trkA - genetics | Oncogene Proteins, Fusion - antagonists & inhibitors | Aged | Carcinoma, Non-Small-Cell Lung - drug therapy | Indazoles - adverse effects | Colorectal Neoplasms - pathology | Protein-Tyrosine Kinases - antagonists & inhibitors | Index Medicus
Journal Article
The New England Journal of Medicine, ISSN 0028-4793, 01/2012, Volume 366, Issue 1, pp. 20 - 33
In this trial, vorapaxar, a protease-activated–receptor 1 antagonist that inhibits thrombin-induced platelet activation, was not effective in reducing the... 
MEDICINE, GENERAL & INTERNAL | DESIGN | GLYCOPROTEIN IIB/IIIA INHIBITORS | CLOPIDOGREL | RATIONALE | DOUBLE-BLIND | PHASE-II | PLACEBO-CONTROLLED TRIAL | ST-SEGMENT ELEVATION | ASPIRIN | ANTIPLATELET THERAPY | Follow-Up Studies | Angioplasty | Cardiovascular Diseases - prevention & control | Humans | Middle Aged | Male | Pyridines - adverse effects | Cardiovascular Diseases - mortality | Female | Drug Therapy, Combination | Platelet Aggregation Inhibitors - therapeutic use | Platelet Aggregation Inhibitors - adverse effects | Pyridines - therapeutic use | Double-Blind Method | Receptor, PAR-1 - antagonists & inhibitors | Kaplan-Meier Estimate | Combined Modality Therapy | Lactones - adverse effects | Lactones - therapeutic use | Acute Coronary Syndrome - drug therapy | Intracranial Hemorrhages - chemically induced | Coronary Artery Bypass | Acute Coronary Syndrome - therapy | Aged | Hemorrhage - chemically induced | Antagonists (Biochemistry) | Drugs | Dose-response relationship (Biochemistry) | Dosage and administration | Product/Service Evaluations | Drug therapy | Coronary heart disease | Myocardial infarction | Cerebral infarction | Stroke | Heart attacks | Proteinase-activated receptor 1 | Thrombin | Cardiovascular disease | Hemorrhage | Bleeding | Investigations | Manuscripts | Ischemia | Blood platelets | Acute coronary syndromes | Research centers | Index Medicus | Abridged Index Medicus | Malalties cardiovasculars | Bypass cardiopulmonar | Medicaments | Bypass cardiopulmonary | Plaquetes sanguínies | Cardiovascular diseases | Kardiologi | Clinical Medicine | Cardiac and Cardiovascular Systems | Medical and Health Sciences | Klinisk medicin | Medicin och hälsovetenskap
Journal Article
Science, ISSN 0036-8075, 9/2010, Volume 329, Issue 5997, pp. 1345 - 1348
Although practiced clinically for more than 40 years, the use of hematopoietic stem cell (HSC) transplants remains limited by the ability to expand these cells... 
Hep G2 cells | Cytokines | REPORTS | Stem cells | Multipotent stem cells | Bone marrow | Cultured cells | Transplantation | Aryl hydrocarbon receptors | Hematopoietic stem cells | Blood | EX-VIVO EXPANSION | ENGRAFTMENT | MULTIDISCIPLINARY SCIENCES | BONE-MARROW | BIOLOGY | MICE | UMBILICAL-CORD BLOOD | BINDING | TRANSPLANTATION | Antigens, CD34 - analysis | Cell Proliferation | Receptors, Aryl Hydrocarbon - antagonists & inhibitors | Species Specificity | Cell Count | Humans | Aryl Hydrocarbon Hydroxylases - genetics | Antigens, CD - analysis | Multipotent Stem Cells - drug effects | Hematopoiesis | Polychlorinated Dibenzodioxins - pharmacology | Hematopoietic Stem Cells - physiology | Receptors, Aryl Hydrocarbon - metabolism | Multipotent Stem Cells - physiology | Hematopoietic Stem Cells - drug effects | Signal Transduction | Purines - metabolism | Purines - pharmacology | Cells, Cultured | Hematopoietic Stem Cell Transplantation | Hematopoietic Stem Cells - metabolism | Mice, SCID | AC133 Antigen | Aryl Hydrocarbon Hydroxylases - metabolism | Cell Lineage | Animals | Multipotent Stem Cells - cytology | Small Molecule Libraries | Hematopoietic Stem Cells - cytology | Cytochrome P-450 CYP1B1 | Mice, Inbred NOD | Mice | Glycoproteins - analysis | Cytokines - pharmacology | Peptides - analysis | Physiological aspects | Arylation | Human | Receptors | Aromatic compounds | Modulation | Hydrocarbons | Derivatives | Culture | Index Medicus
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