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Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 08/2016, Volume 36, Issue 8, pp. 1525 - 1533
OBJECTIVE—The role of hypercoagulability in the pathogenesis of diabetic nephropathy (DN) remains elusive. We recently reported the increased infiltration of... 
cardiovascular diseases | factor Xa | inflammation | prognosis | diabetic nephropathy | CELLS | INJURY | FACTOR-VII | PATHWAY | ROLES | PERIPHERAL VASCULAR DISEASE | MICE | HEMATOLOGY | EXPRESSION | CONTRIBUTES | TISSUE FACTOR | Up-Regulation | Humans | Receptor, PAR-2 - metabolism | Male | Receptor, PAR-2 - deficiency | Nitric Oxide Synthase Type III - deficiency | Receptor, PAR-2 - antagonists & inhibitors | Inflammation Mediators - metabolism | Kidney Glomerulus - metabolism | Factor Xa Inhibitors - pharmacology | Insulin - genetics | Cytokines - genetics | Diabetic Nephropathies - prevention & control | Disease Models, Animal | Receptor, PAR-2 - genetics | Cell Line | Diabetic Nephropathies - pathology | Factor Xa - genetics | Podocytes - metabolism | Cytokines - metabolism | Anti-Inflammatory Agents - pharmacology | Endothelial Cells - metabolism | Diabetic Nephropathies - metabolism | Kidney Glomerulus - drug effects | Diabetic Nephropathies - genetics | Genotype | Kidney Glomerulus - pathology | Nitric Oxide Synthase Type III - genetics | Factor Xa - metabolism | Mice, Knockout | Macrophages - metabolism | Phenotype | Animals | Blood Coagulation - drug effects | Podocytes - drug effects | Signal Transduction - drug effects | Macrophages - drug effects | Pyridines - pharmacology | Thiazoles - pharmacology | Factor Xa - drug effects | Endothelial Cells - drug effects
Journal Article
Nature, ISSN 0028-0836, 05/2017, Volume 545, Issue 7652, pp. 112 - 115
Protease-activated receptors ( PARs) are a family of G-proteincoupled receptors ( GPCRs) that are irreversibly activated by proteolytic cleavage of the N... 
PHENIX | THROMBIN | CRYSTAL-STRUCTURE | MULTIDISCIPLINARY SCIENCES | Allosteric Regulation - drug effects | Benzyl Alcohols - chemistry | Allosteric Site - drug effects | Humans | Receptor, PAR-2 - metabolism | Imidazoles - chemistry | Models, Molecular | Crystallography, X-Ray | Antibodies, Blocking - pharmacology | Imidazoles - pharmacology | Benzimidazoles - chemistry | Receptor, PAR-2 - chemistry | Immunoglobulin Fab Fragments - pharmacology | Receptor, PAR-2 - antagonists & inhibitors | Signal Transduction - drug effects | Antibodies, Blocking - chemistry | Immunoglobulin Fab Fragments - chemistry | Benzyl Alcohols - pharmacology | Benzimidazoles - pharmacology | Ligands | Benzodioxoles - chemistry | Kinetics | Benzodioxoles - pharmacology | Physiological aspects | Cell receptors | Allosteric proteins | Cytochrome | Residues | G protein-coupled receptors | Peptides | Molecular structure | Hydrogen | Homology | Antagonists | Hydrophobicity | Hydrogen bonding | Optimization | Proteins | Lipophilic | Allosteric properties | Imidazole | Cleavage | Inhibition | Thromboembolism | Lysozyme | Hydrogen ion concentration | Deoxyribonucleic acid--DNA | Cultivation | Architecture | Fab | Crystals | Crystallization | Pharmacology | Inflammation | Glycosylation | Computer programs | Chemistry | Diffraction | Antagonist drugs | Lysine | Isoforms | Computer applications | Mutation | Internet | Receptor mechanisms | Binding sites | Glutamine | Cancer
Journal Article
Journal Article
Nature, ISSN 0028-0836, 03/2012, Volume 483, Issue 7391, pp. 627 - 631
Journal Article
Pain, ISSN 0304-3959, 05/2015, Volume 156, Issue 5, pp. 859 - 867
Protease-activated receptor type 2 (PAR(2)) is known to play an important role in inflammatory, visceral, and cancer-evoked pain based on studies using PAR(2)... 
PAR | Proteinase activated receptor | Hyperalgesic priming | BDNF | Translation control | Atypical PKC | MAPK | NMDA RECEPTORS | NEUROTROPHIC FACTOR | PKM-ZETA | NEUROSCIENCES | DORSAL-HORN | CLINICAL NEUROLOGY | NEUROPATHIC PAIN | NOCICEPTIVE PLASTICITY | ANESTHESIOLOGY | CANCER PAIN | PROTEASE-ACTIVATED-RECEPTOR-2 SENSITIZES | INFLAMMATORY PAIN | Hyperalgesia - chemically induced | Brain-Derived Neurotrophic Factor - antagonists & inhibitors | Chronic Pain - chemically induced | Nitriles - pharmacology | Receptor, PAR-2 - metabolism | Male | Hyperalgesia - psychology | Receptor, PAR-2 - deficiency | Receptor, PAR-2 - antagonists & inhibitors | Receptor, trkB - antagonists & inhibitors | Behavior, Animal - drug effects | Benzamides - pharmacology | Brain-Derived Neurotrophic Factor - metabolism | Disease Models, Animal | Dinoprostone - pharmacology | Butadienes - pharmacology | Chronic Pain - drug therapy | Hyperalgesia - metabolism | Mice, Inbred C57BL | Facial Expression | Protein Kinase C - antagonists & inhibitors | Chronic Pain - psychology | Mice, Inbred ICR | Hydrazones - pharmacology | Mice, Knockout | Azepines - pharmacology | Chronic Pain - metabolism | Animals | MAP Kinase Signaling System - drug effects | Hyperalgesia - drug therapy | Signal Transduction - drug effects | Receptor, PAR-2 - agonists | Mice | Thiazoles - pharmacology | proteinase activated receptor | atypical PKC | PAR2 | translation control
Journal Article
JOURNAL OF BIOLOGICAL CHEMISTRY, ISSN 0021-9258, 08/2017, Volume 292, Issue 33, pp. 13688 - 13701
Cell migration and invasion are very characteristic features of cancer cells that promote metastasis, which is one of the most common causes of mortality among... 
EPITHELIAL-MESENCHYMAL TRANSITION | MIGRATION | CELLS | CYCLIN D1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | PROTEINS | EXPRESSION | BINDING | TISSUE FACTOR | INSIGHTS | Phosphatidylinositol 3-Kinase - antagonists & inhibitors | Humans | Receptor, PAR-2 - metabolism | Neoplasm Proteins - antagonists & inhibitors | Neoplasm Proteins - metabolism | Breast - metabolism | Proto-Oncogene Proteins c-akt - genetics | Thromboplastin - agonists | Breast Neoplasms - metabolism | Breast Neoplasms - enzymology | Factor VIIIa - metabolism | Receptor, PAR-2 - antagonists & inhibitors | RNA Interference | Neoplasm Invasiveness - pathology | Female | Glycogen Synthase Kinase 3 beta - chemistry | Gene Expression Regulation, Neoplastic - drug effects | Neoplasm Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | Breast - pathology | Phosphatidylinositol 3-Kinase - metabolism | Receptor, PAR-2 - genetics | Recombinant Proteins - metabolism | Breast - cytology | beta Catenin - agonists | Enzyme Inhibitors - pharmacology | Recombinant Proteins - chemistry | Glycogen Synthase Kinase 3 beta - antagonists & inhibitors | Factor VIIIa - genetics | Glycogen Synthase Kinase 3 beta - metabolism | beta Catenin - metabolism | beta Catenin - genetics | Phosphatidylinositol 3-Kinase - chemistry | Cell Movement - drug effects | Neoplasm Proteins - agonists | Signal Transduction - drug effects | Breast Neoplasms - pathology | beta Catenin - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - agonists | Thromboplastin - genetics | Receptor, PAR-2 - agonists | Cell Line, Tumor | Genes, Reporter - drug effects | Thromboplastin - metabolism | Oligopeptides - pharmacology | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | coagulation factor | β-catenin | breast cancer | signaling | Signal Transduction | tissue factor
Journal Article
Nature, ISSN 0028-0836, 03/2018, Volume 555, Issue 7698, pp. 673 - 677
Obesity-induced metabolic disease involves functional integration among several organs via circulating factors, but little is known about crosstalk between... 
TISSUE INFLAMMATION | DIPEPTIDYL PEPTIDASE-4 INHIBITOR | GLYCEMIC CONTROL | DOSE-RESPONSE | LINKING OBESITY | MACROPHAGES | MULTIDISCIPLINARY SCIENCES | ENDOTHELIAL-CELLS | BODY-MASS INDEX | TYPE-2 DIABETES-MELLITUS | EXPRESSION | Dipeptidyl Peptidase 4 - metabolism | Sitagliptin Phosphate - pharmacology | Humans | Receptor, PAR-2 - metabolism | Male | Hepatocytes - metabolism | Receptor, PAR-2 - deficiency | Obesity - genetics | Inflammation - metabolism | Hepatocytes - drug effects | Receptor, PAR-2 - genetics | Sitagliptin Phosphate - administration & dosage | Administration, Oral | Caveolin 1 - genetics | Caveolin 1 - deficiency | Dipeptidyl Peptidase 4 - genetics | Intra-Abdominal Fat - metabolism | Factor Xa - metabolism | Obesity - metabolism | Caveolin 1 - metabolism | Macrophages - metabolism | Animals | Dipeptidyl Peptidase 4 - deficiency | Insulin Resistance - genetics | Inflammation - genetics | Mice, Obese | Mice | Obesity - enzymology | Intra-Abdominal Fat - pathology | Inflammation - enzymology | Hepatocytes - enzymology | Physiological aspects | Obesity | Insulin resistance | Observations | Caveolin-1 | Peptidase | Adipose tissue | Caveolin | Liver | Crosstalk | Oral administration | Organs | Inflammation | Kinases | Macrophages | Insulin | Proteins | Disease resistance | Functional integration | Hepatocytes | Rodents
Journal Article
British Journal of Pharmacology, ISSN 0007-1188, 09/2016, Volume 173, Issue 18, pp. 2752 - 2765
Journal Article