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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
Nature Communications, ISSN 2041-1723, 12/2019, Volume 10, Issue 1, pp. 1897 - 1897
The cellular decision regarding whether to undergo proliferation or death is made at the restriction (R)-point, which is disrupted in nearly all tumors. The... 
UBIQUITINATION | AML1-ETO | ACETYLATION | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | PROTEINS | QUANTITATIVE-ANALYSIS | POLYCOMB | CANCER | KINASES | FAMILY | Chromatin - metabolism | RNA, Small Interfering - genetics | Myeloid-Lymphoid Leukemia Protein - metabolism | TOR Serine-Threonine Kinases - metabolism | Core Binding Factor Alpha 3 Subunit - antagonists & inhibitors | Humans | Polycomb-Group Proteins - metabolism | TOR Serine-Threonine Kinases - genetics | Cell Cycle Checkpoints - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Chromatin - chemistry | MAP Kinase Kinase 1 - antagonists & inhibitors | Butadienes - pharmacology | Signal Transduction | Epithelial Cells - pathology | MAP Kinase Kinase 1 - metabolism | Imidazoles - pharmacology | Cyclin-Dependent Kinase 4 - metabolism | Piperazines - pharmacology | Cell Cycle Checkpoints - drug effects | Polycomb-Group Proteins - genetics | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cell Line, Tumor | MAP Kinase Kinase 4 - genetics | RNA, Small Interfering - metabolism | ras Proteins - genetics | Core Binding Factor Alpha 3 Subunit - metabolism | Epithelial Cells - metabolism | Nitriles - pharmacology | Cyclin-Dependent Kinase 4 - genetics | Epithelial Cells - drug effects | ras Proteins - metabolism | Drosophila melanogaster - genetics | Chromatin Assembly and Disassembly - drug effects | Drosophila melanogaster - metabolism | MAP Kinase Kinase 1 - genetics | TOR Serine-Threonine Kinases - antagonists & inhibitors | MAP Kinase Kinase 4 - metabolism | HEK293 Cells | MAP Kinase Kinase 4 - antagonists & inhibitors | Chromatin - drug effects | Histone-Lysine N-Methyltransferase - genetics | Drosophila melanogaster - cytology | Gene Expression Regulation | p38 Mitogen-Activated Protein Kinases - genetics | Sirolimus - pharmacology | Animals | Histone-Lysine N-Methyltransferase - metabolism | Myeloid-Lymphoid Leukemia Protein - genetics | Core Binding Factor Alpha 3 Subunit - genetics | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Pyridines - pharmacology | Index Medicus
Journal Article
Biochemical Journal, ISSN 0264-6021, 04/2013, Volume 451, Issue 2, pp. 313 - 328
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
Journal of Biological Chemistry, ISSN 0021-9258, 08/2015, Volume 290, Issue 32, pp. 19900 - 19909
Accumulating evidence suggests that activation of mitogen-activated protein kinases (MAPKs) and nuclear factor NF-kappa B exacerbates early brain injury (EBI)... 
SIGNALING PATHWAYS | VASOSPASM | LEARNING-DEFICITS | PHOSPHORYLATION | INFLAMMATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | GROWTH | MECHANISMS | NF-KAPPA-B | EXPRESSION | PROTECTS | Neurons - pathology | Phosphorylation | Transcription Factor RelA - antagonists & inhibitors | Apoptosis - drug effects | Injections, Intraventricular | Male | Cerebrovascular Trauma - metabolism | I-kappa B Proteins - metabolism | I-kappa B Proteins - genetics | Transcription Factor RelA - genetics | Anti-Inflammatory Agents, Non-Steroidal - pharmacology | MAP Kinase Kinase 4 - metabolism | Neuroprotective Agents - pharmacology | I-kappa B Proteins - antagonists & inhibitors | MAP Kinase Kinase 4 - antagonists & inhibitors | Neurons - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | MAP Kinase Kinase Kinases - antagonists & inhibitors | Neurons - drug effects | Subarachnoid Hemorrhage - drug therapy | Disease Models, Animal | NF-KappaB Inhibitor alpha | Signal Transduction | MAP Kinase Kinase Kinases - genetics | Gene Expression Regulation | Rats | p38 Mitogen-Activated Protein Kinases - genetics | Zearalenone - analogs & derivatives | MAP Kinase Kinase Kinases - metabolism | Subarachnoid Hemorrhage - genetics | Subarachnoid Hemorrhage - pathology | Rats, Sprague-Dawley | Stereotaxic Techniques | Subarachnoid Hemorrhage - metabolism | Animals | Transcription Factor RelA - metabolism | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cerebrovascular Trauma - pathology | MAP Kinase Kinase 4 - genetics | Cerebrovascular Trauma - prevention & control | Protein Kinase Inhibitors - pharmacology | Cerebrovascular Trauma - genetics | Zearalenone - pharmacology | Index Medicus | TAK1 | neuroprotection | 5Z-7-oxozeaenol | subarachnoid hemorrhage | Neurobiology | mitogen-activated protein kinase (MAPK) | apoptosis | brain | NF-κB (NF-KB)
Journal Article
Scientific Reports, ISSN 2045-2322, 12/2018, Volume 8, Issue 1, pp. 857 - 10
Journal Article
by Pek, M and Yatim, S.M.J.M and Chen, Y and Li, J and Gong, M and Jiang, X and Zhang, F and Zheng, J and Wu, X and Yu, Q
Oncogene, ISSN 0950-9232, 08/2017, Volume 36, Issue 35, pp. 4975 - 4986
Therapeutic strategies against KRAS mutant colorectal cancers are developed using cell line models, which do not accurately represent the transcriptome driven... 
BIOCHEMISTRY & MOLECULAR BIOLOGY | PANCREATIC-CANCER | DNA-DAMAGE | TRANSCRIPTION | SYNTHETIC LETHAL INTERACTION | PROLIFERATION | FOXM1 | SUPPRESSION | CELL BIOLOGY | RECEPTOR TYROSINE KINASES | MUTATION STATUS | ONCOLOGY | GENETICS & HEREDITY | CELL-CYCLE | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Diphenylamine - pharmacology | Proto-Oncogene Proteins p21(ras) - genetics | Colorectal Neoplasms - genetics | Cyclin-Dependent Kinase 4 - genetics | Humans | Gene Expression Profiling | Molecular Targeted Therapy | Diphenylamine - analogs & derivatives | Colorectal Neoplasms - drug therapy | Female | Benzamides - pharmacology | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | MAP Kinase Kinase Kinases - antagonists & inhibitors | Proto-Oncogene Proteins p21(ras) - metabolism | Colorectal Neoplasms - enzymology | MAP Kinase Kinase Kinases - genetics | HCT116 Cells | Cyclin-Dependent Kinase 6 - genetics | Cyclin-Dependent Kinase 6 - metabolism | MAP Kinase Kinase Kinases - metabolism | Random Allocation | Cyclin-Dependent Kinase 4 - metabolism | Mice, SCID | Piperazines - pharmacology | HT29 Cells | Xenograft Model Antitumor Assays | Animals | Cell Line, Tumor | Mice, Inbred NOD | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Pyridines - pharmacology | Care and treatment | Research | Gene mutations | Gene expression | Colorectal cancer | Cell cycle | Cell culture | Toxicity | Epithelial cells | Mitosis | Colorectal carcinoma | Cancer therapies | Cyclin-dependent kinase 4 | K-Ras protein | Metastases | Xenografts | Mutation | Colon | Tumors | Index Medicus
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 12/2007, Volume 117, Issue 12, pp. 4044 - 4054
Targeting kinases is central to drug-based cancer therapy but remains challenging because the drugs often lack specificity, which may cause toxic side effects.... 
CHRONIC MYELOGENOUS LEUKEMIA | MEDICINE, RESEARCH & EXPERIMENTAL | GASTROINTESTINAL STROMAL TUMOR | ACTIVATION | PROTEIN-TYROSINE KINASES | STI571 | PHOSPHORYLATION | IMATINIB | STI-571 INHIBITION | PROLIFERATION | CANCER-THERAPY | Gastrointestinal Stromal Tumors - enzymology | Protein-Tyrosine Kinases - metabolism | Humans | Neoplasms, Experimental - enzymology | Piperazines - chemistry | Protein Kinase Inhibitors - adverse effects | Proto-Oncogene Proteins c-kit - metabolism | Pyrimidines - chemistry | Protein Kinase Inhibitors - chemistry | MAP Kinase Kinase 4 - metabolism | Fusion Proteins, bcr-abl | MAP Kinase Kinase 4 - antagonists & inhibitors | Heart Diseases - chemically induced | Cardiotoxins - pharmacology | Rats | Pyrimidines - pharmacology | Heart Diseases - enzymology | Imatinib Mesylate | Piperazines - adverse effects | Piperazines - pharmacology | Rats, Sprague-Dawley | Animals | Gastrointestinal Stromal Tumors - drug therapy | K562 Cells | Pyrimidines - adverse effects | Protein Kinase Inhibitors - pharmacology | Benzamides | Cardiotoxins - chemistry | Neoplasms, Experimental - drug therapy | Drug Screening Assays, Antitumor | Protein-Tyrosine Kinases - antagonists & inhibitors | Care and treatment | Research | Protein kinases | Health aspects | Methods | Cancer | Index Medicus | Abridged Index Medicus | Technical Advance
Journal Article
Oncogene, ISSN 0950-9232, 06/2017, Volume 36, Issue 23, pp. 3334 - 3345
Despite remarkable progress in cutaneous melanoma genomic profiling, the mutational landscape of primary mucosal melanomas (PMM) remains unclear. Forty-six... 
TARGETED THERAPY | MUTANT MELANOMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | IMPROVED SURVIVAL | CANCER | CELL BIOLOGY | MUTATED MELANOMA | GENE FUSIONS | MEK INHIBITION | ONCOLOGY | GENETICS & HEREDITY | RAF INHIBITORS | MUTATIONS | SEQUENCING DATA | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Oncogene Proteins, Fusion - metabolism | Skin Neoplasms - drug therapy | Apoptosis - drug effects | Cyclin-Dependent Kinase 4 - genetics | Humans | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | MAP Kinase Kinase 1 - genetics | Biomarkers, Tumor - metabolism | Female | Antineoplastic Agents - pharmacology | Mucous Membrane - drug effects | Tumor Cells, Cultured | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Proto-Oncogene Proteins B-raf - metabolism | Melanoma - metabolism | Skin Neoplasms - pathology | MAP Kinase Kinase 1 - antagonists & inhibitors | Cyclin-Dependent Kinase 6 - genetics | MAP Kinase Kinase 1 - metabolism | Cyclin-Dependent Kinase 6 - metabolism | Melanoma - pathology | Transcription Factors - genetics | Cyclin-Dependent Kinase 4 - metabolism | Mucous Membrane - metabolism | Skin Neoplasms - metabolism | Phosphatidylinositol 3-Kinases - genetics | Transcription Factors - metabolism | Xenograft Model Antitumor Assays | Mucous Membrane - pathology | Animals | Mice, Nude | Oncogene Proteins, Fusion - genetics | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Biomarkers, Tumor - genetics | Cell Proliferation - drug effects | Mice | Mitogen-Activated Protein Kinases - metabolism | Care and treatment | Gene mutations | Melanoma | Development and progression | Cellular signal transduction | Genetic aspects | Health aspects | Index Medicus
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
International Immunopharmacology, ISSN 1567-5769, 09/2011, Volume 11, Issue 9, pp. 1166 - 1172
(AS), an herb used in traditional Chinese medicine, is thought to have anti-inflammatory activities. Ligustilide is its most abundant ingredient. This study... 
Mitogen-activated protein kinase | Activator protein-1 | Ligustilide | Nitric oxide | Nuclear factor κB | ACTIVATION | NITRIC-OXIDE SYNTHASE | DYSMENORRHEA | IMMUNOLOGY | ENDOMETRIOSIS | Nuclear factor kappa B | ISOBENZOFURANONE | PATHOGENESIS | ANTIOXIDANT | PHARMACOLOGY & PHARMACY | TNF-ALPHA | ANGELICA-SINENSIS | PROSTAGLANDIN E-2 | Nitric Oxide Synthase Type II - biosynthesis | Reactive Oxygen Species - metabolism | Transcription Factor RelA - antagonists & inhibitors | Dinoprostone - biosynthesis | Transcription Factor AP-1 - genetics | Transcription Factor AP-1 - metabolism | Transcription Factor RelA - genetics | Mitogen-Activated Protein Kinase Kinases - metabolism | I-kappa B Kinase - metabolism | I-kappa B Kinase - antagonists & inhibitors | Nitric Oxide Synthase Type II - antagonists & inhibitors | MAP Kinase Kinase 4 - antagonists & inhibitors | Phosphorylation - drug effects | Cell Line | Nitric Oxide - biosynthesis | Nitric Oxide - antagonists & inhibitors | 4-Butyrolactone - pharmacology | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | I-kappa B Kinase - genetics | Down-Regulation - drug effects | Macrophages - enzymology | Macrophages - metabolism | Reactive Oxygen Species - antagonists & inhibitors | Transcription Factor AP-1 - antagonists & inhibitors | Animals | MAP Kinase Signaling System - drug effects | Nitric Oxide Synthase Type II - genetics | Signal Transduction - drug effects | Transcription Factor RelA - metabolism | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Lipopolysaccharides - pharmacology | Macrophages - drug effects | Mice | 4-Butyrolactone - analogs & derivatives | Dinoprostone - antagonists & inhibitors | Tumor Necrosis Factor-alpha - biosynthesis | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Index Medicus
Journal Article
Journal of the National Cancer Institute, ISSN 0027-8874, 05/2017, Volume 109, Issue 5
Journal Article