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Circulation Research, ISSN 0009-7330, 01/2009, Volume 104, Issue 1, pp. 15 - 18
Ischemic postconditioning (IPoC) reduces infarct size following ischemia/reperfusion. Whether or not phosphorylation of RISK (reperfusion injury salvage... 
PERMEABILITY TRANSITION PORE | CARDIAC & CARDIOVASCULAR SYSTEMS | PROTECTION | REPERFUSION | reperfusion injury | NECROSIS-FACTOR-ALPHA | ADENOSINE RECEPTORS | infarct size | INHIBITION | MYOCARDIAL INFARCT SIZE | cardioprotection | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | MOUSE HEARTS | SIGNAL TRANSDUCER | Glycogen Synthase Kinase 3 - physiology | MAP Kinase Kinase 2 - physiology | Nitriles - pharmacology | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Glycogen Synthase Kinase 3 beta | Ribosomal Protein S6 Kinases, 70-kDa - physiology | MAP Kinase Kinase 1 - physiology | Myocardial Reperfusion Injury - enzymology | Ribosomal Protein S6 Kinases, 70-kDa - biosynthesis | Protein Processing, Post-Translational - drug effects | Swine | Mitogen-Activated Protein Kinase 3 - biosynthesis | Myocardial Infarction - pathology | Swine, Miniature | Phosphorylation - drug effects | Myocardial Infarction - enzymology | MAP Kinase Kinase 1 - antagonists & inhibitors | Butadienes - pharmacology | Glycogen Synthase Kinase 3 - biosynthesis | Mitogen-Activated Protein Kinase 1 - physiology | Glycogen Synthase Kinase 3 - antagonists & inhibitors | Ribosomal Protein S6 Kinases, 70-kDa - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Coronary Occlusion - enzymology | Enzyme Induction | Proto-Oncogene Proteins c-akt - physiology | Enzyme Activation - drug effects | Mitogen-Activated Protein Kinase 3 - physiology | Mitogen-Activated Protein Kinase 1 - biosynthesis | Proto-Oncogene Proteins c-akt - biosynthesis | Animals | Androstadienes - pharmacology | Myocardial Reperfusion | MAP Kinase Kinase 2 - antagonists & inhibitors | Coronary Occlusion - pathology | Phosphatidylinositol 3-Kinases - physiology | Protein Kinase Inhibitors - pharmacology | Myocardial Reperfusion Injury - prevention & control | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Index Medicus
Journal Article
Nature chemical biology, ISSN 1552-4450, 10/2014, Volume 10, Issue 10, pp. 853 - 860
Activation of the ERK pathway is a hallmark of cancer, and targeting of upstream signaling partners led to the development of approved drugs. Recently,... 
POLY(ADP-RIBOSE) POLYMERASE | RAF INHIBITION | BIOCHEMISTRY & MOLECULAR BIOLOGY | DNA-DAMAGE | ACQUIRED-RESISTANCE | MAP KINASE ERK2 | BRAF | CONFORMATION | MEK INHIBITORS | SELECTIVITY | DISCOVERY | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Gene Expression Regulation, Neoplastic | Intracellular Signaling Peptides and Proteins - metabolism | Piperazines - chemistry | Mitogen-Activated Protein Kinase 1 - chemistry | Enzyme Inhibitors - chemistry | Mitogen-Activated Protein Kinase 1 - genetics | Mitogen-Activated Protein Kinase 8 - genetics | Antineoplastic Agents - pharmacology | Mitogen-Activated Protein Kinase 3 - chemistry | Binding Sites | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Protein Structure, Tertiary | Recombinant Proteins - metabolism | Gene Expression | Indazoles - chemistry | Mitogen-Activated Protein Kinase 3 - genetics | Protein Structure, Secondary | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 8 - chemistry | Mitogen-Activated Protein Kinase 8 - metabolism | Enzyme Inhibitors - pharmacology | Protein-Serine-Threonine Kinases - genetics | Recombinant Proteins - chemistry | Recombinant Proteins - genetics | Antineoplastic Agents - chemistry | Piperazines - pharmacology | Indazoles - pharmacology | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Intracellular Signaling Peptides and Proteins - chemistry | Cell Line, Tumor | Protein Binding | Protein-Serine-Threonine Kinases - chemistry | Kinetics | Mitogen-Activated Protein Kinase 1 - metabolism | Signal transduction | Binding sites | Pharmaceutical sciences | Cancer | Index Medicus
Journal Article
Science, ISSN 0036-8075, 4/2011, Volume 332, Issue 6027, pp. 358 - 361
Transforming growth factor—β (TGFβ) signaling drives aneurysm progression in multiple disorders, including Marfan syndrome (MFS), and therapies that inhibit... 
Transcriptional regulatory elements | Echocardiography | Aortic diseases | Root growth | REPORTS | Placebos | Aneurysms | Aorta | Mice | Aortic aneurysm | Marfan syndrome | PATHOGENESIS | CELLS | ACTIVATION | VALSALVA | MULTIDISCIPLINARY SCIENCES | N-TERMINAL KINASE | MOUSE MODEL | NOONANS-SYNDROME | RECEPTOR | MUTATIONS | INHIBITOR | Diphenylamine - pharmacology | Aortic Aneurysm - metabolism | Mitogen-Activated Protein Kinase 8 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Anthracenes - therapeutic use | MAP Kinase Signaling System | Diphenylamine - analogs & derivatives | Marfan Syndrome - drug therapy | Smad4 Protein - genetics | Transforming Growth Factor beta - antagonists & inhibitors | Aortic Aneurysm - pathology | Aortic Aneurysm - prevention & control | Disease Models, Animal | Transforming Growth Factor beta - immunology | Diphenylamine - therapeutic use | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 8 - metabolism | Aortic Aneurysm - physiopathology | Losartan - pharmacology | Smad2 Protein - metabolism | Sulfonamides - pharmacology | Anthracenes - pharmacology | Disease Progression | Aorta - pathology | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Sulfonamides - therapeutic use | Protein Kinase Inhibitors - therapeutic use | Losartan - therapeutic use | Marfan Syndrome - metabolism | Marfan Syndrome - pathology | Protein Kinase Inhibitors - pharmacology | Smad4 Protein - deficiency | Enzyme Activation | Transforming Growth Factor beta - metabolism | Mitogen-Activated Protein Kinase 1 - metabolism | Index Medicus | Therapy | Progressions | Pathways | Strategy | Activation | Inhibition | Kinases
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 02/2005, Volume 288, Issue 2, pp. 971 - 976
Pharmacological activation of the prosurvival kinases Akt and ERK-1/2 at reperfusion, after a period of lethal ischemia, protects the heart against... 
Myocardial infarction | Phosphatidylinositol 3-kinase-Akt | Reperfusion injury | Mitogen-activated protein kinases | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | phosphatidylinositol 3-kinase-Akt | HEARTS | myocardial infarction | INJURY | reperfusion injury | MITOCHONDRIAL PERMEABILITY TRANSITION | mitogen-activated protein kinases | PORE | PERIPHERAL VASCULAR DISEASE | RADICALS | Phosphorylation | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Male | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Myocardial Reperfusion Injury - pathology | Myocardial Infarction - pathology | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Survival - physiology | Protein-Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins - metabolism | MAP Kinase Kinase 1 - antagonists & inhibitors | Proto-Oncogene Proteins - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Enzyme Inhibitors - pharmacology | Rats | MAP Kinase Kinase 1 - metabolism | Myocardium - pathology | MAP Kinase Kinase 2 - metabolism | Myocardial Infarction - metabolism | Rats, Sprague-Dawley | Proto-Oncogene Proteins c-akt | Myocardial Reperfusion Injury - metabolism | Myocardium - enzymology | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Ischemic Preconditioning, Myocardial | MAP Kinase Kinase 2 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - metabolism | Index Medicus
Journal Article
Experimental Cell Research, ISSN 0014-4827, 10/2012, Volume 318, Issue 16, pp. 2105 - 2115
The activation of transforming growth factor-β1(TGF-β1)/Smad signaling pathway and increased expression of connective tissue growth factor (CTGF) induced by... 
TGFβ1 | Angiotensin II | Atrial fibroblasts | TRAF6 | CTGF | MAPKs | TGFΒ1 | Heart Atria - pathology | Gene Expression - drug effects | Heart Atria - drug effects | Transforming Growth Factor beta1 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Transforming Growth Factor beta1 - metabolism | TNF Receptor-Associated Factor 6 - antagonists & inhibitors | Fibrosis - metabolism | MAP Kinase Kinase 4 - metabolism | Mitogen-Activated Protein Kinase 1 - genetics | MAP Kinase Kinase 4 - antagonists & inhibitors | p38 Mitogen-Activated Protein Kinases - metabolism | TNF Receptor-Associated Factor 6 - genetics | MAP Kinase Kinase Kinases - antagonists & inhibitors | Fibroblasts - metabolism | Angiotensin II - pharmacology | Fibrosis - genetics | Mitogen-Activated Protein Kinase 3 - genetics | MAP Kinase Kinase Kinases - genetics | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Losartan - pharmacology | p38 Mitogen-Activated Protein Kinases - genetics | MAP Kinase Kinase Kinases - metabolism | Signal Transduction - genetics | Transforming Growth Factor beta1 - genetics | Fibroblasts - pathology | Heart Atria - metabolism | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Signal Transduction - drug effects | Fibroblasts - drug effects | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | TNF Receptor-Associated Factor 6 - metabolism | MAP Kinase Kinase 4 - genetics | Connective Tissue Growth Factor - genetics | Mice | Protein Kinase Inhibitors - pharmacology | Primary Cell Culture | Angiotensin II - physiology | Connective Tissue Growth Factor - metabolism | Mitogen-Activated Protein Kinase 1 - metabolism | Index Medicus
Journal Article
Journal of Cell Science, ISSN 0021-9533, 2013, Volume 126, Issue 17, pp. 3990 - 3999
The crucial role the Crumbs and Par polarity complexes play in tight junction integrity has long been established, however very few studies have investigated... 
Scribble | Polarity | Tight junctions | Mammary epithelium | EMT | ERK | CELL-CELL JUNCTIONS | PROTEIN-KINASE-C | BARRIER FUNCTION | E-CADHERIN | MAMMALIAN EPITHELIAL-CELLS | BETA-CATENIN | MESENCHYMAL TRANSITION | TIGHT JUNCTION | CELL BIOLOGY | MALIGNANT PROGRESSION | TUMOR-SUPPRESSOR SCRIBBLE | MAP Kinase Signaling System - physiology | Phosphorylation | Epithelial-Mesenchymal Transition - physiology | Homeodomain Proteins - metabolism | Humans | Membrane Glycoproteins - biosynthesis | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Transcriptional Activation | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | RNA Interference | Mitogen-Activated Protein Kinase 1 - genetics | HEK293 Cells | Transcription, Genetic | Flavonoids - pharmacology | Membrane Proteins - metabolism | Chromones - pharmacology | Tight Junctions - metabolism | MAP Kinase Kinase 1 - antagonists & inhibitors | Tumor Suppressor Proteins - metabolism | Homeodomain Proteins - biosynthesis | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - genetics | Down-Regulation | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Morpholines - pharmacology | Transcription Factors - antagonists & inhibitors | Transcription Factors - biosynthesis | Anthracenes - pharmacology | Transcription Factors - metabolism | Membrane Proteins - biosynthesis | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Homeodomain Proteins - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | RNA, Small Interfering | Tumor Suppressor Proteins - biosynthesis | Mitogen-Activated Protein Kinase 1 - metabolism | Zinc Finger E-box-Binding Homeobox 1 | Index Medicus
Journal Article
Science, ISSN 0036-8075, 2/2007, Volume 315, Issue 5814, pp. 1000 - 1003
Pathogenic bacteria use the type III secretion system to deliver effector proteins into host cells to modulate the host signaling pathways. In this study, the... 
Phosphates | Phosphorylation | Phosphatases | HeLa cells | Mass spectroscopy | Immunoblotting | Bacteria | Reports | Infections | Chemical bonding | Family members | SHIGELLA-FLEXNERI | CELLS | ACTIVATION | VIRULENCE PLASMID | MULTIDISCIPLINARY SCIENCES | SECRETION SYSTEM | HOST | INFECTION | EXPRESSION | Shigella flexneri - metabolism | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Phosphoprotein Phosphatases - metabolism | Molecular Sequence Data | JNK Mitogen-Activated Protein Kinases - metabolism | NF-kappa B - metabolism | Salmonella typhimurium | MAP Kinase Signaling System | p38 Mitogen-Activated Protein Kinases - metabolism | Amino Acid Sequence | Cell Line | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Bacterial Proteins - genetics | Tyrosine - metabolism | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mutagenesis | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Bacterial Proteins - metabolism | HeLa Cells | Shigella flexneri - physiology | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism | Physiological aspects | Immune response | Gram-negative bacteria | Research | Secretion | Enzymes | Pathogens | Biochemistry | Kinases | Spectrum analysis | Index Medicus
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 12/2007, Volume 117, Issue 12, pp. 4003 - 4008
Phosphate homeostasis is maintained by a counterbalance between efflux from the kidney and influx from intestine and bone. FGF23 is a bone-derived phosphaturic... 
PHOSPHATE | MEDICINE, RESEARCH & EXPERIMENTAL | HORMONE GENE-EXPRESSION | IN-VIVO | CALCIUM | GROWTH | KLOTHO PROTEIN | SECONDARY HYPERPARATHYROIDISM | VITAMIN-D-RECEPTOR | DOMINANT HYPOPHOSPHATEMIC RICKETS | MICE | MAP Kinase Signaling System - physiology | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Fibroblast Growth Factors - genetics | Intestines - metabolism | Parathyroid Hormone - genetics | Fibroblast Growth Factors - metabolism | Parathyroid Glands - cytology | RNA, Messenger - biosynthesis | Kidney - metabolism | Parathyroid Hormone - biosynthesis | Bone and Bones - metabolism | Mitogen-Activated Protein Kinase 1 - genetics | Early Growth Response Protein 1 - genetics | Receptors, Fibroblast Growth Factor - genetics | Homeostasis - drug effects | Mitogen-Activated Protein Kinase 3 - genetics | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | RNA, Messenger - genetics | Cells, Cultured | Gene Expression Regulation - physiology | Rats | Fibroblast Growth Factors - pharmacology | Gene Expression Regulation - drug effects | Phosphates - metabolism | Animals | Glucuronidase - biosynthesis | MAP Kinase Signaling System - drug effects | Early Growth Response Protein 1 - biosynthesis | Glucuronidase - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Homeostasis - physiology | Receptors, Fibroblast Growth Factor - metabolism | Vitamin D - metabolism | Protein Kinase Inhibitors - pharmacology | Mitogen-Activated Protein Kinase 1 - metabolism | Parathyroid Glands - metabolism | Homeostasis | Parathyroid glands | Fibroblast growth factors | Dosage and administration | Genetic aspects | Research | Health aspects | Index Medicus | Abridged Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 12/2016, Volume 11, Issue 12, pp. e0167071 - e0167071
Background Cigarette smoking plays an important role in the progression of chronic kidney disease (CKD). Nicotine, one of the major components of cigarette... 
ACETYLCHOLINE-RECEPTORS | CIGARETTE-SMOKING | NMDA RECEPTORS | RISK-FACTOR | MULTIDISCIPLINARY SCIENCES | RENAL-FUNCTION | INJURY | DIABETIC-NEPHROPATHY | CHRONIC KIDNEY-DISEASE | CARDIOVASCULAR MORBIDITY | ROS PRODUCTION | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Apoptosis - genetics | Male | Nicotinic Antagonists - pharmacology | Spin Labels | Reactive Oxygen Species - agonists | Nicotine - pharmacology | MAP Kinase Kinase 4 - metabolism | Cyclic N-Oxides - pharmacology | Mitogen-Activated Protein Kinase 1 - genetics | Female | MAP Kinase Kinase 4 - antagonists & inhibitors | Membrane Proteins - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Receptors, Nicotinic - metabolism | Podocytes - metabolism | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Membrane Proteins - genetics | Tissue Culture Techniques | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Gene Expression Regulation | p38 Mitogen-Activated Protein Kinases - genetics | Nicotine - antagonists & inhibitors | Podocytes - cytology | Reactive Oxygen Species - antagonists & inhibitors | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Podocytes - drug effects | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Acetylcysteine - pharmacology | MAP Kinase Kinase 4 - genetics | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Oxidative Stress - drug effects | Receptors, Nicotinic - genetics | Cell Line, Transformed | Mitogen-Activated Protein Kinase 1 - metabolism | Oxidative stress | Physiological aspects | Research | Health aspects | Health/Alcohol and other Drugs/Information/Nicotine and Tobacco | Nicotine | Smoking | Apoptosis | Cell proliferation | Reactive oxygen species | Phosphorylation | Laboratories | Syngeneic grafts | Downstream effects | Tempol | Acetylcysteine | Superoxide dismutase | Antagonists | mRNA | Medical schools | Antioxidants | Proteins | Receptors | Rodents | Mesangial cells | Localization | Medical research | Extracellular signal-regulated kinase | JNK protein | Superoxide | Permeability | Gene expression | Cigarette smoking | Signaling | Molecular modelling | Inhibitors | Acetylcholine receptors (nicotinic) | In vivo methods and tests | Acetylcholine | Kidney diseases | Diabetes | Kidney transplantation | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2015, Volume 10, Issue 4, pp. e0124007 - e0124007
Cell invasion is a crucial mechanism of cancer metastasis and malignancy. Matrix metallo-proteinase-9 (MMP-9) is an important proteolytic enzyme involved in... 
MATRIX METALLOPROTEINASES | ANGIOGENESIS | NUCLEAR-FACTOR | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | INDUCED MATRIX-METALLOPROTEINASE-9 EXPRESSION | CYCLOOXYGENASE-2 EXPRESSION | PROLIFERATION | FOS | C-JUN | NF-KAPPA-B | Phosphorylation | Epithelial Cells - metabolism | Tetradecanoylphorbol Acetate - pharmacology | Mitogen-Activated Protein Kinase 8 - antagonists & inhibitors | Transcription Factor AP-1 - genetics | Epithelial Cells - drug effects | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Gene Expression Regulation, Neoplastic | Gastric Mucosa - metabolism | Mitogen-Activated Protein Kinase 9 - genetics | Tetradecanoylphorbol Acetate - antagonists & inhibitors | Transcription Factor AP-1 - metabolism | Dose-Response Relationship, Drug | Matrix Metalloproteinase 9 - metabolism | Matrix Metalloproteinase 9 - genetics | Oligodeoxyribonucleotides - genetics | Mitogen-Activated Protein Kinase 1 - genetics | Mitogen-Activated Protein Kinase 8 - genetics | Flavonoids - pharmacology | Stomach - drug effects | Oligodeoxyribonucleotides - metabolism | Stomach - pathology | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Mitogen-Activated Protein Kinase 9 - metabolism | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 8 - metabolism | Proto-Oncogene Proteins c-fos - metabolism | Epithelial Cells - pathology | Antibodies - pharmacology | Cell Movement - drug effects | Transcription Factor AP-1 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - metabolism | Mitogen-Activated Protein Kinase 9 - antagonists & inhibitors | Cell Line, Tumor | Proto-Oncogene Proteins c-fos - genetics | Antineoplastic Agents, Phytogenic - pharmacology | Mitogen-Activated Protein Kinase 1 - metabolism | Enzymes | Care and treatment | Oligodeoxynucleotides | Stomach cancer | Cancer cells | Cancer | Transcription factors | Oligonucleotides | Malignancy | Metastasis | Matrix metalloproteinase | Kinases | Cancer therapies | Medical schools | Western blotting | Metastases | Anticancer properties | Angiogenesis | Signal transduction | Pathways | Fos protein | Proteolysis | Metalloproteinase | c-Fos protein | Gastric cancer | Invasiveness | Extracellular signal-regulated kinase | c-Jun protein | Blocking | Breast cancer | Gene expression | Gelatinase B | Polymerase chain reaction | Signaling | Acetic acid | Index Medicus
Journal Article
Journal of Bone and Mineral Research, ISSN 0884-0431, 04/2011, Volume 26, Issue 4, pp. 730 - 738
Mesenchymal stem cells (MSCs) cultured on extracellular matrices with different stiffness have been shown to possess diverse lineage commitment owing to the... 
mesenchymal stem cell | matrix stiffness | integrin | mechanotransduction | osteogenic differentiation | MATRIX STIFFNESS | OSTEOBLAST DIFFERENTIATION | GROWTH-HORMONE | INTEGRIN | ENDOCRINOLOGY & METABOLISM | OSTEOGENIC DIFFERENTIATION | FOCAL ADHESION KINASE | LINEAGE | MESENCHYMAL STEM CELL | RHOA | MECHANOTRANSDUCTION | RNA, Small Interfering - genetics | Osteogenesis - physiology | Gene Expression - drug effects | Gene Expression - genetics | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Collagen Type I - chemistry | Osteocalcin - genetics | Acrylic Resins - chemical synthesis | Integrin alpha2 - metabolism | Mechanotransduction, Cellular - physiology | rho-Associated Kinases - antagonists & inhibitors | Elasticity - physiology | Mesenchymal Stromal Cells - cytology | Collagen Type I - genetics | rho-Associated Kinases - metabolism | Extracellular Matrix - physiology | Myosin-Light-Chain Phosphatase - metabolism | Osteoblasts - cytology | Phosphorylation - drug effects | Cell Differentiation - physiology | Focal Adhesion Kinase 1 - metabolism | Mesenchymal Stromal Cells - drug effects | Calcification, Physiologic - drug effects | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Osteoblasts - drug effects | Calcification, Physiologic - physiology | Mesenchymal Stromal Cells - metabolism | Acrylic Resins - chemistry | beta Catenin - metabolism | Biomechanical Phenomena | Integrin alpha2 - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Cell Differentiation - drug effects | Protein Kinase Inhibitors - pharmacology | Osteoblasts - metabolism | Focal Adhesion Kinase 1 - antagonists & inhibitors | Core Binding Factor Alpha 1 Subunit - genetics | Mitogen-Activated Protein Kinase 1 - metabolism | Index Medicus
Journal Article
Journal Article
Free Radical Biology and Medicine, ISSN 0891-5849, 09/2017, Volume 110, pp. 291 - 299
Mounting evidence demonstrated deficient cystathionine-γ-lyase (CSE)/H S implicated the development of cardiovascular disease. The present study aimed to... 
Hydrogen sulfide | TXNIP | Endothelial function | MAPK | CELLS | OXIDATIVE STRESS | ANGIOGENESIS | NITRIC-OXIDE SYNTHASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CYSTATHIONINE-GAMMA-LYASE | ATHEROSCLEROSIS | THIOREDOXIN-INTERACTING PROTEIN | INFLAMMATION | ENDOCRINOLOGY & METABOLISM | CARDIOVASCULAR-DISEASE | HYPERTENSION | Human Umbilical Vein Endothelial Cells | Hydrogen Sulfide - metabolism | Glycine - analogs & derivatives | RNA, Small Interfering - genetics | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Endothelium, Vascular - drug effects | Aorta - metabolism | MAP Kinase Kinase 4 - metabolism | Thioredoxins - genetics | Mitogen-Activated Protein Kinase 1 - genetics | Alkynes - pharmacology | MAP Kinase Kinase 4 - antagonists & inhibitors | Thioredoxins - metabolism | Thioredoxins - antagonists & inhibitors | p38 Mitogen-Activated Protein Kinases - metabolism | Cystathionine gamma-Lyase - genetics | Nitric Oxide Synthase Type III - metabolism | Cystathionine gamma-Lyase - deficiency | Sulfides - pharmacology | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Aorta - drug effects | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Carrier Proteins - antagonists & inhibitors | Gene Expression Regulation | p38 Mitogen-Activated Protein Kinases - genetics | Nitric Oxide Synthase Type III - genetics | Mice, Knockout | Aorta - pathology | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Glycine - pharmacology | Mitogen-Activated Protein Kinase 3 - metabolism | Endothelium, Vascular - metabolism | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | MAP Kinase Kinase 4 - genetics | Endothelium, Vascular - pathology | Mice | Protein Kinase Inhibitors - pharmacology | Mitogen-Activated Protein Kinase 1 - metabolism | RNA, Small Interfering - metabolism | Medical research | Nitric oxide | Medicine, Experimental | Acetylcholine | Thioredoxin | Protein kinases | Endothelium | Index Medicus
Journal Article