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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
Abstract Paclitaxel chemotherapy is limited by a long-lasting painful neuropathy that lacks an effective therapy. In this study, we tested the hypothesis that... 
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 | SENSORY NEURONS | CAPSAICIN RECEPTOR | MECHANICAL HYPERALGESIA | IN-VIVO | KINASE-C-EPSILON | ION-CHANNEL | PERIPHERAL NEUROPATHY | INFLAMMATORY PAIN | PROTEASE-ACTIVATED-RECEPTOR-2 SENSITIZES | IRRITABLE-BOWEL-SYNDROME | 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 | Neurosciences | Paclitaxel | Phospholipases | Protein kinases | Cancer
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2. 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 and Klinisk kemi and Linköpings universitet and Institutionen för klinisk och experimentell medicin and Diagnostikcentrum and Östergötlands Läns Landsting and Hälsouniversitetet and Avdelningen för mikrobiologi och molekylär medicin
Pigment Cell & Melanoma Research, ISSN 1755-1471, 05/2014, Volume 27, Issue 3, pp. 431 - 441
Summary The proteinase‐activated receptor 1 (PAR‐1) plays a central role in melanoma progression and its expression level is believed to correlate with the... 
gene expression regulation | microRNAs | melanoma | proteinase‐activated receptor‐1 | metastasis | Proteinase-activated receptor-1 | Gene expression regulation | Metastasis | MicroRNAs | Melanoma | TARGET | TUMOR-CELLS | IDENTIFICATION | CANCER | MICRORNA CLUSTER | CELL BIOLOGY | DERMATOLOGY | MESSENGER-RNA | GENE | ONCOLOGY | COAGULATION | proteinase-activated receptor-1 | TISSUE FACTOR | 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 | melanoma; metastasis; proteinase-activated receptor-1; gene expression regulation; microRNAs | Medical and Health Sciences | MEDICINE | Medicin och hälsovetenskap | MEDICIN
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3. 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, 04/2017, Volume 15, Issue 4, pp. 597 - 607
Summary Idiopathic pulmonary fibrosis (IPF) is a lethal lung disease with a 5‐year mortality rate of > 50% and unknown etiology. Treatment options remain... 
anticoagulants | fibrosis | idiopathic pulmonary fibrosis | receptor, PAR‐1 | receptor, PAR‐2 | receptors, proteinase‐activated | receptor, PAR-2 | receptor, PAR-1 | receptors, proteinase-activated | PAR-2 | PAR-1 | receptors | LIVER FIBROSIS | EPITHELIAL-MESENCHYMAL TRANSITION | INTERSTITIAL LUNG-DISEASE | receptor | ANTICOAGULANT-THERAPY | proteinase-activated | POTENTIAL-ROLE | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | THROMBIN RECEPTOR | UP-REGULATION | TISSUE FACTOR | AFFORDS PROTECTION | ACUTE EXACERBATION | 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
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4. 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
Proteinase-activated receptors (PARs) are a subfamily of G protein-coupled receptors (GPCRs) with four members, PAR(1), PAR(2), PAR(3) and PAR(4), playing... 
ISCHEMIA-REPERFUSION INJURY | GROWTH-FACTOR RECEPTOR | PROSTAGLANDIN E-2 RELEASE | LUNG EPITHELIAL-CELLS | LIGAND-DERIVED PEPTIDES | POTENTIAL VANILLOID 4 | RESONANCE ENERGY-TRANSFER | CYCLOOXYGENASE-2 UP-REGULATION | VASCULAR SMOOTH-MUSCLE | MOUSE ISOLATED TRACHEA | 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
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5. 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
Journal of Neuroscience, ISSN 0270-6474, 05/2004, Volume 24, Issue 18, pp. 4293 - 4299
Proteinase-activated receptor (PAR) 2 is expressed on a subset of primary afferent neurons and involved in inflammatory nociception. Transient receptor... 
PKC | Proteinase-activated receptor | TRPV1 | Thermal hyperalgesia | Inflammatory pain | Mechanical allodynia | thermal hyperalgesia | proteinase-activated receptor | INVOLVEMENT | KINASE-C | CAPSAICIN-RECEPTOR | NEUROSCIENCES | RAT PAW | PATHWAY | PROTECTIVE ROLE | NEURONS | inflammatory pain | mechanical allodynia | MOLECULAR-CLONING | GROWTH-FACTOR | THROMBIN RECEPTOR | 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 | Cellular | Molecular
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6. 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 and Medicinska fakulteten and Medicinska och farmaceutiska vetenskapsområdet and Uppsala universitet and Institutionen för medicinska vetenskaper and Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm and Uppsala kliniska forskningscentrum (UCR)
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 | PLACEBO | GLYCOPROTEIN IIB/IIIA INHIBITORS | CLOPIDOGREL | TASK-FORCE | SAFETY | DOUBLE-BLIND | 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 | 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
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7. Full Text Role of Spinal Neurotransmitter Receptors in Itch: New Insights into Therapies and Drug Development
by Cevikbas, Ferda and Steinhoff, Martin and Ikoma, Akihiko
CNS Neuroscience & Therapeutics, ISSN 1755-5930, 12/2011, Volume 17, Issue 6, pp. 742 - 749
SUMMARY Targets for antipruritic therapies are now expanding from the skin to the central nervous system. Recent studies demonstrate that various neuronal... 
Histamine | Itch | Spinal cord | Neurokinin‐1 receptor | Gastrin‐releasing peptide | Opioid | Skin | Pruritus | Neurokinin-1 receptor | Gastrin-releasing peptide | DORSAL-HORN NEURONS | PROTEINASE-ACTIVATED RECEPTOR-2 | GENE-RELATED PEPTIDE | KAPPA-OPIOID RECEPTORS | VASOACTIVE-INTESTINAL-PEPTIDE | INTRATHECAL MORPHINE | HISTAMINE H-1 RECEPTORS | NEUROSCIENCES | PHARMACOLOGY & PHARMACY | MORPHINE-INDUCED ITCH | INDUCED SCRATCHING BEHAVIOR | SUBSTANCE-P RECEPTOR | Receptors, Histamine - physiology | Receptors, Serotonin - physiology | Gastrin-Secreting Cells - physiology | Receptors, Bradykinin - physiology | Humans | Receptors, Serotonin - drug effects | Receptors, Histamine - drug effects | Receptors, Bradykinin - drug effects | Receptors, Neurokinin-1 - physiology | Receptors, Glutamate - drug effects | Pruritus - physiopathology | Receptors, Opioid - physiology | Receptors, Neurokinin-1 - drug effects | Animals | Pruritus - drug therapy | Spinal Cord - physiology | Drug Design | Neurotransmitter Agents - physiology | Receptors, Opioid - drug effects | Receptors, Glutamate - physiology | Gastrin-Secreting Cells - drug effects | Antihistamines | Methyl aspartate | Gabapentin | Dermatology | Sulfonamides | Bradykinin | Formulae, receipts, prescriptions | Gastrin | Dermatologic agents | Glutamate | Drugs | pruritus | Opioid receptors | Glutamic acid receptors (ionotropic) | Substance P | Central nervous system | Opioid receptors (type mu) | N-Methyl-D-aspartic acid receptors | Antagonists | Glutamic acid receptors | Drug development | Side effects | gabapentin | Neurotransmission | Dorsal horn
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