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1. Full Text Proteinase-activated receptor 2 sensitizes transient receptor potential vanilloid 1, transient receptor potential vanilloid 4, and transient receptor potential ankyrin 1 in paclitaxel-induced neuropathic pain
by Chen, Y and Yang, C and Wang, Z.J
Neuroscience, ISSN 0306-4522, 2011, Volume 193, pp. 440 - 451
Neurology | mast cell tryptase | paclitaxel-induced pain | TRPV1 | TRPA1 | proteinase-activated receptor 2 | TRPV4 | Proteinase-activated receptor 2 | Mast cell tryptase | Paclitaxel-induced pain | Neurosciences | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Fundamental and applied biological sciences. Psychology | Vertebrates: nervous system and sense organs | Biological and medical sciences | Tryptases - metabolism | Central Nervous System - metabolism | Capsaicin - pharmacology | Receptor, PAR-2 - metabolism | Type C Phospholipases - metabolism | Male | Neuralgia - pathology | Dose-Response Relationship, Drug | TRPV Cation Channels - metabolism | Receptor, PAR-2 - antagonists & inhibitors | Drug Interactions | Paclitaxel - toxicity | Time Factors | Protein Kinase C - metabolism | TRPV Cation Channels - antagonists & inhibitors | Estrenes - pharmacology | Pyrrolidinones - pharmacology | Neuralgia - chemically induced | Neuralgia - physiopathology | Disease Models, Animal | Cyclic AMP-Dependent Protein Kinases - metabolism | Enzyme Inhibitors - pharmacology | Capsaicin - analogs & derivatives | Sulfonamides - pharmacology | Cinnamates - pharmacology | Mice, Inbred ICR | Hyperalgesia - physiopathology | Antineoplastic Agents, Phytogenic - toxicity | Gene Expression Regulation - drug effects | Pain Measurement - methods | Pyrroles - pharmacology | Animals | Analysis of Variance | Ankyrins - antagonists & inhibitors | Anilides - pharmacology | Ankyrins - metabolism | Central Nervous System - drug effects | Mice | Physical Stimulation - adverse effects | Carbazoles - pharmacology | Oligopeptides - pharmacology | Protein Kinase C - pharmacology | Enzymes | Care and treatment | Paclitaxel | Phospholipases | Protein kinases | Cancer | Index Medicus
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2. Full Text Targeting coagulation factor receptors - protease-activated receptors in idiopathic pulmonary fibrosis
by Lin, C and Borensztajn, K and Spek, C. A
Journal of thrombosis and haemostasis, ISSN 1538-7933, 2017, Volume 15, Issue 4, pp. 597 - 607
anticoagulants | fibrosis | idiopathic pulmonary fibrosis | receptor, PAR‐1 | receptor, PAR‐2 | receptors, proteinase‐activated | receptor, PAR-2 | receptor, PAR-1 | receptors, proteinase-activated | Peripheral Vascular Disease | Life Sciences & Biomedicine | Hematology | Cardiovascular System & Cardiology | Science & Technology | Anticoagulants | Receptors, Proteinase-Activated - metabolism | Receptor, PAR-1 - antagonists & inhibitors | Humans | Inflammation | Disease Progression | Idiopathic Pulmonary Fibrosis - metabolism | Lactones - therapeutic use | Receptors, Proteinase-Activated - antagonists & inhibitors | Receptor, PAR-2 - antagonists & inhibitors | Animals | Bleomycin - chemistry | Blood Coagulation - drug effects | Idiopathic Pulmonary Fibrosis - mortality | Blood Coagulation Factors - therapeutic use | Mice | Fibrosis - pathology | Platelet Aggregation Inhibitors - therapeutic use | Disease Models, Animal | Pyridines - therapeutic use | Respiratory tract diseases | Development and progression | Pulmonary fibrosis | Proteases | Pharmaceutical industry | Coagulation | Index Medicus
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3. Full Text Proteinase-activated receptors (PARs) - Focus on receptor-receptor- interactions and their physiological and pathophysiological impact
by Gieseler, Frank and Ungefroren, Hendrik and Settmacher, Utz and Hollenberg, Morley D and Kaufmann, Roland
Cell communication and signaling, ISSN 1478-811X, 2013, Volume 11, Issue 1, pp. 86 - 86
Life Sciences & Biomedicine | Science & Technology | Cell Biology | Neoplasms - metabolism | Receptor Cross-Talk | Cardiovascular Diseases - metabolism | Receptors, G-Protein-Coupled - metabolism | Signal Transduction | Humans | Protein Multimerization | Transcriptional Activation | Protein-Serine-Threonine Kinases - genetics | Molecular Targeted Therapy | Pain - metabolism | Receptor Protein-Tyrosine Kinases - metabolism | Arrestins - metabolism | Protein Transport | Receptors, Proteinase-Activated - physiology | Inflammation - metabolism | Animals | Receptor Protein-Tyrosine Kinases - genetics | beta-Arrestins | Protein-Serine-Threonine Kinases - metabolism | Tyrosine | Cell interaction | Cell receptors | Proteases | Cellular signal transduction | G proteins | Thrombosis | Blood clot | Index Medicus
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4. Full Text miR‐20b regulates expression of proteinase‐activated receptor‐1 (PAR‐1) thrombin receptor in melanoma cells
by Saleiban, Amina and Faxälv, Lars and Claesson, Kjersti and Jönsson, Jan‐Ingvar and Osman, Abdimajid
Pigment cell and melanoma research, ISSN 1755-1471, 05/2014, Volume 27, Issue 3, pp. 431 - 441
gene expression regulation | microRNAs | melanoma | proteinase‐activated receptor‐1 | metastasis | Proteinase-activated receptor-1 | Gene expression regulation | Metastasis | MicroRNAs | Melanoma | Oncology | Life Sciences & Biomedicine | Dermatology | Science & Technology | Cell Biology | MicroRNAs - antagonists & inhibitors | Humans | 3' Untranslated Regions - genetics | RNA, Neoplasm - isolation & purification | RNA, Messenger - metabolism | MicroRNAs - isolation & purification | Thrombin - biosynthesis | Melanoma - genetics | Neoplasm Proteins - genetics | Calcium Signaling | Gene Expression Regulation, Neoplastic - genetics | Genes, Reporter | Melanoma - metabolism | RNA Processing, Post-Transcriptional | Neoplasm Proteins - biosynthesis | RNA, Messenger - genetics | Gene Silencing | Melanoma - secondary | Receptor, PAR-1 - genetics | Receptor, PAR-1 - biosynthesis | Cell Line, Tumor | RNA, Neoplasm - genetics | MicroRNAs - genetics | MicroRNAs - physiology | Neoplasm Invasiveness - genetics | Thrombin | MicroRNA | Gene expression | Antigen presentation | Index Medicus
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5. Full Text Thrombin-Receptor Antagonist Vorapaxar in Acute Coronary Syndromes
by Tricoci, Pierluigi and Huang, Zhen and Held, Claes and Moliterno, David J and Armstrong, Paul W and Van de Werf, Frans and White, Harvey D and Aylward, Philip E and Wallentin, Lars and Chen, Edmond and Lokhnygina, Yuliya and Pei, Jinglan and Leonardi, Sergio and Rorick, Tyrus L and Kilian, Ann M and Jennings, Lisa H.K and Ambrosio, Giuseppe and Bode, Christoph and Cequier, Angel and Cornel, Jan H and Diaz, Rafael and Erkan, Aycan and Huber, Kurt and Hudson, Michael P and Jiang, Lixin and Jukema, J. Wouter and Lewis, Basil S and Lincoff, A. Michael and Montalescot, Gilles and Nicolau, José Carlos and Ogawa, Hisao and Pfisterer, Matthias and Prieto, Juan Carlos and Ruzyllo, Witold and Sinnaeve, Peter R and Storey, Robert F and Valgimigli, Marco and Whellan, David J and Widimsky, Petr and Strony, John and Harrington, Robert A and Mahaffey, Kenneth W and TRACER Investigators
The New England journal of medicine, ISSN 0028-4793, 01/2012, Volume 366, Issue 1, pp. 20 - 33
Medicine, General & Internal | Life Sciences & Biomedicine | General & Internal Medicine | Science & Technology | Cardiology. Vascular system | Heart | General aspects | Biological and medical sciences | Myocarditis. Cardiomyopathies | Medical sciences | Coronary heart disease | 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 | 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
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6. Full Text Proteinase-Activated Receptor 2-Mediated Potentiation of Transient Receptor Potential Vanilloid Subfamily 1 Activity Reveals a Mechanism for Proteinase-Induced Inflammatory Pain
by Dai, Yi and Moriyama, Tomoko and Higashi, Tomohiro and Togashi, Kazuya and Kobayashi, Kimiko and Yamanaka, Hiroki and Tominaga, Makoto and Noguchi, Koichi
The Journal of neuroscience, ISSN 0270-6474, 05/2004, Volume 24, Issue 18, pp. 4293 - 4299
PKC | Proteinase-activated receptor | TRPV1 | Thermal hyperalgesia | Inflammatory pain | Mechanical allodynia | Neurosciences | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Neurons - pathology | Temperature | Spinal Cord - metabolism | Receptor, PAR-1 - metabolism | Receptors, Drug - genetics | Humans | Receptor, PAR-2 - metabolism | Male | Transfection | Pain - enzymology | Protein Kinase C - metabolism | Spinal Cord - pathology | Receptors, Drug - deficiency | Neurons - metabolism | Neurons - drug effects | Receptor, PAR-2 - genetics | Endopeptidases - metabolism | Mice, Inbred C57BL | Cells, Cultured | Enzyme Inhibitors - pharmacology | Proto-Oncogene Proteins c-fos - metabolism | Protein Kinase C - antagonists & inhibitors | Receptor, PAR-1 - genetics | Receptors, Drug - metabolism | Hyperalgesia - physiopathology | Mice, Knockout | Patch-Clamp Techniques | Animals | Receptors, Thrombin - genetics | Hyperalgesia - genetics | Pain - physiopathology | Ganglia, Spinal - pathology | Receptor, PAR-2 - agonists | Receptors, Thrombin - metabolism | Signal Transduction - physiology | Mice | Inflammation - enzymology | Ganglia, Spinal - metabolism | Inflammation - physiopathology | Index Medicus | thermal hyperalgesia | Cellular | proteinase-activated receptor | inflammatory pain | mechanical allodynia | Molecular
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