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The Lancet (British edition), ISSN 0140-6736, 2009, Volume 373, Issue 9678, pp. 1905 - 1917
...) expression, raised macrophage migration inhibitory factor, and increased P-glycoprotein-mediated drug efflux... 
Internal Medicine | Medicine, General & Internal | Life Sciences & Biomedicine | General & Internal Medicine | Science & Technology | Transcription Factor AP-1 - drug effects | Glucocorticoids - therapeutic use | Transcriptional Activation - genetics | Transcription Factor AP-1 - genetics | Humans | Macrophage Migration-Inhibitory Factors - immunology | Transcriptional Activation - drug effects | Transcription Factor AP-1 - immunology | Histone Deacetylases - immunology | Transcriptional Activation - immunology | ATP-Binding Cassette, Sub-Family B, Member 1 - drug effects | Calcineurin Inhibitors | Macrophage Migration-Inhibitory Factors - genetics | Inflammation - drug therapy | Phosphodiesterase 4 Inhibitors | Anti-Inflammatory Agents - therapeutic use | Mitogen-Activated Protein Kinases - immunology | Genetic Predisposition to Disease - genetics | NF-kappa B - antagonists & inhibitors | Histone Deacetylases - genetics | Macrophage Migration-Inhibitory Factors - drug effects | Repressor Proteins - genetics | Histone Deacetylase 2 | Drug Resistance - drug effects | Inflammation - immunology | Asthma - drug therapy | ATP-Binding Cassette, Sub-Family B, Member 1 - immunology | Drug Resistance - genetics | ATP-Binding Cassette, Sub-Family B, Member 1 - genetics | Drug Resistance - immunology | Repressor Proteins - immunology | Histone Deacetylases - drug effects | Mitogen-Activated Protein Kinases - genetics | Repressor Proteins - drug effects | Mitogen-Activated Protein Kinases - drug effects | Pulmonary Disease, Chronic Obstructive - drug therapy | Corticosteroids | Dosage and administration | Inflammation | Research | Drug resistance | Drug therapy | Health aspects | Complications and side effects | Risk factors | Inflammatory bowel disease | Proteins | Respiratory distress syndrome | Asthma | Steroids | Index Medicus | Abridged Index Medicus
Journal Article
Journal of endodontics, ISSN 0099-2399, 05/2014, Volume 40, Issue 5, pp. 640 - 647
Journal Article
Diabetes (New York, N.Y.), ISSN 1939-327X, 04/2017, Volume 66, Issue 4, pp. 908 - 919
Journal Article
by Meng, S and Zhang, L and Tang, Y and Tu, Q and Zheng, L and Yu, L and Murray, D and Cheng, J and Kim, S.H and Zhou, X and Chen, J
Journal of dental research, ISSN 1544-0591, 05/2014, Volume 93, Issue 7, pp. 657 - 662
Journal Article
Gastroenterology (New York, N.Y. 1943), ISSN 0016-5085, 06/2014, Volume 146, Issue 7, pp. 1763 - 1774
..., NLRP3, and caspase-1 (CASP1); release of IL1β; and activation of nuclear factor-κB (NF-κB) and caspase-1. Small interfering RNAs were used to reduce levels of GPR81 and arrestin... 
Gastroenterology and Hepatology | Innate Immune Response | Immune Regulation | Pancreas | Mouse Model | Gastroenterology & Hepatology | Life Sciences & Biomedicine | Science & Technology | Liver - pathology | Inflammasomes - metabolism | Receptors, G-Protein-Coupled - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Male | NF-kappa B - metabolism | Monocytes - immunology | Lipopolysaccharides | Liver - immunology | Liver - drug effects | RNA Interference | Interleukin-1beta - metabolism | Toll-Like Receptors - drug effects | Anti-Inflammatory Agents - administration & dosage | Toll-Like Receptors - metabolism | Cytoprotection | Disease Models, Animal | Galactosamine | Chemical and Drug Induced Liver Injury - prevention & control | Anti-Inflammatory Agents - pharmacology | Down-Regulation | Liver - metabolism | Injections, Intraperitoneal | Pancreas - pathology | Pancreas - metabolism | Pancreas - immunology | Toll-Like Receptor 4 - metabolism | Chemical and Drug Induced Liver Injury - immunology | Monocytes - drug effects | Macrophages - metabolism | Signal Transduction - drug effects | Chemical and Drug Induced Liver Injury - metabolism | Sodium Lactate - pharmacology | beta-Arrestins | Mice | Receptors, G-Protein-Coupled - genetics | RNA, Small Interfering - metabolism | Monocytes - metabolism | Pancreatitis - prevention & control | Arrestins - metabolism | Dose-Response Relationship, Drug | Pancreatitis - genetics | Transfection | Inflammasomes - drug effects | Sodium Lactate - administration & dosage | Pancreatitis - immunology | Chemical and Drug Induced Liver Injury - pathology | Chemical and Drug Induced Liver Injury - etiology | Macrophages - immunology | Cell Line | Immunity, Innate - drug effects | Toll-Like Receptor 4 - drug effects | Mice, Inbred C57BL | Pancreas - drug effects | Chemical and Drug Induced Liver Injury - genetics | Pancreatitis - chemically induced | Animals | Carrier Proteins - metabolism | beta-Arrestin 2 | Inflammasomes - immunology | Macrophages - drug effects | Pancreatitis - pathology | Pancreatitis - metabolism | Ceruletide | Lactates | Gastrointestinal diseases | Inflammation | Index Medicus | Abridged Index Medicus
Journal Article
PloS one, ISSN 1932-6203, 01/2013, Volume 8, Issue 1, pp. e50175 - e50175
Bladder cancer is the most common malignant urological disease in China. Hydroxycamptothecin (HCPT) is a DNA topoisomerase I inhibitor, which has been utilized... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Apoptosis - drug effects | Humans | NF-kappa B - metabolism | DNA-Binding Proteins - metabolism | Dose-Response Relationship, Drug | Topoisomerase I Inhibitors - pharmacology | G2 Phase Cell Cycle Checkpoints - drug effects | Urinary Bladder Neoplasms - genetics | I-kappa B Kinase - metabolism | Tumor Suppressor Proteins - genetics | Urinary Bladder Neoplasms - pathology | Cell Cycle Proteins - genetics | DNA Fragmentation - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Urinary Bladder Neoplasms - metabolism | Protein-Serine-Threonine Kinases - metabolism | Camptothecin - analogs & derivatives | Tumor Suppressor Proteins - metabolism | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Ataxia Telangiectasia Mutated Proteins | I-kappa B Kinase - genetics | Urinary Bladder Neoplasms - drug therapy | DNA-Binding Proteins - genetics | Drug Synergism | Xenograft Model Antitumor Assays | Animals | NF-kappa B - genetics | Signal Transduction - drug effects | Mice, Nude | Genistein - pharmacology | Cell Line, Tumor | Mice | Antineoplastic Agents, Phytogenic - pharmacology | Camptothecin - pharmacology | Drug Resistance, Neoplasm - drug effects | Flow cytometry | Biotechnology | Epithelial cells | DNA damage | Genistein | Colorectal cancer | Bladder | Cytotoxicity | Activation | Retailing | Urology | Angiogenesis | Cell growth | Urinary bladder | Rodents | Xenografts | Cell cycle | Biocompatibility | Ataxia | Tumorigenesis | Pretreatment | Deoxyribonucleic acid--DNA | Isoflavones | NF-κB protein | DNA topoisomerase | Tumor cell lines | Cervix | Bladder cancer | Chemotherapy | Molecular modelling | Ataxia telangiectasia mutated protein | Females | Prostate cancer | Prostate | Cervical cancer | Apoptosis | Cancer | Index Medicus | Deoxyribonucleic acid | DNA
Journal Article
Cancer letters, ISSN 0304-3835, 02/2015, Volume 357, Issue 2, pp. 520 - 526
Abstract Although mutations of p53 and KRAS and activation of NF-κB signaling have been highly associated with chemoresistance and tumorigenesis of lung cancer, the interactive mechanisms between two of p53, KRAS, and NF-κB are elusive... 
Hematology, Oncology and Palliative Medicine | NF-κB | KRAS | Lung cancer | Chemoresistance | p53 | P53 | Life Sciences & Biomedicine | Oncology | Science & Technology | Cell Cycle - genetics | Lung Neoplasms - drug therapy | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Paclitaxel - pharmacology | Apoptosis - drug effects | Heterocyclic Compounds, 3-Ring - pharmacology | Humans | Lung Neoplasms - metabolism | ras Proteins - metabolism | Apoptosis - genetics | NF-kappa B - metabolism | Tumor Suppressor Protein p53 - genetics | Cell Nucleus - metabolism | I-kappa B Kinase - metabolism | I-kappa B Kinase - antagonists & inhibitors | Tumor Burden - genetics | Antineoplastic Agents - pharmacology | Lung Neoplasms - genetics | Proto-Oncogene Proteins - metabolism | Carcinogenesis - genetics | Tumor Suppressor Protein p53 - metabolism | Proto-Oncogene Proteins - genetics | Cisplatin - pharmacology | Xenograft Model Antitumor Assays - methods | Blotting, Western | Carcinogenesis - drug effects | Drug Resistance, Neoplasm - genetics | Animals | Transcription Factor RelA - metabolism | Tumor Burden - drug effects | Active Transport, Cell Nucleus - drug effects | Cell Line, Tumor | Mice, Inbred BALB C | Pyridines - pharmacology | Mutation | Cell Cycle - drug effects | Cell Nucleus - drug effects | Drug Resistance, Neoplasm - drug effects | Index Medicus
Journal Article
Journal of the American Heart Association, ISSN 2047-9980, 02/2016, Volume 5, Issue 2, p. n/a
...‐activated protein kinase, extracellular signal–related kinase, and nuclear factor‐κB signaling cascade. These observations were recapitulated in primary human aortic endothelial cells and vascular... 
atherosclerosis | cardiovascular disease | inflammation | endothelial cell | nuclear factor‐κB signaling | vascular smooth muscle cell | leukocyte adhesion | trimethylamine N‐oxide | Endothelial cell | Trimethylamine N-oxide | Nuclear factor-κB signaling | Atherosclerosis | Cardiovascular disease | Leukocyte adhesion | Vascular smooth muscle cell | Inflammation | Cardiac & Cardiovascular Systems | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | Atherosclerosis - genetics | Coculture Techniques | Humans | Myocytes, Smooth Muscle - pathology | Aortitis - enzymology | NF-kappa B - metabolism | Aortitis - chemically induced | Leukocytes - enzymology | Atherosclerosis - enzymology | Receptors, LDL - deficiency | Female | Aortitis - pathology | Myocytes, Smooth Muscle - drug effects | Aorta - enzymology | Disease Models, Animal | Muscle, Smooth, Vascular - drug effects | Receptors, LDL - genetics | Atherosclerosis - pathology | Genetic Predisposition to Disease | Myocytes, Smooth Muscle - enzymology | Aorta - drug effects | Atherosclerosis - chemically induced | Mice, Inbred C57BL | Cells, Cultured | Gene Expression Regulation | Aortitis - genetics | Cell Adhesion - drug effects | Mice, Knockout | Aorta - pathology | Muscle, Smooth, Vascular - pathology | Phenotype | Animals | Signal Transduction - drug effects | Choline | Leukocytes - drug effects | Enzyme Activation | Methylamines - toxicity | Endothelial Cells - pathology | Endothelial Cells - enzymology | Muscle, Smooth, Vascular - enzymology | Endothelial Cells - drug effects | Mitogen-Activated Protein Kinases - metabolism | Index Medicus
Journal Article