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Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 06/2016, Volume 36, Issue 6, pp. 1122 - 1131
OBJECTIVE—The c-Jun NH2-terminal kinases (JNK) are regulated by a wide variety of cellular stresses and have been implicated in apoptotic signaling.... 
atherosclerosis | apoptosis | macrophages | MAP kinase signaling system | endoplasmic reticulum stress | SURVIVAL | ACTIVATION | PHOSPHORYLATION | BAD | SIGNAL-TRANSDUCTION | OBESITY | NH2-TERMINAL KINASE (JNK)1 | INSULIN-RESISTANCE | INFLAMMATION | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | REQUIREMENT | Mitogen-Activated Protein Kinase 8 - antagonists & inhibitors | Apoptosis - drug effects | Bone Marrow Cells - enzymology | Atherosclerosis - genetics | Mitogen-Activated Protein Kinase 9 - genetics | PTEN Phosphohydrolase - antagonists & inhibitors | Atherosclerosis - enzymology | Hypercholesterolemia - enzymology | Diet, High-Fat | Bone Marrow Transplantation | Receptors, LDL - deficiency | bcl-Associated Death Protein - metabolism | Bone Marrow Cells - drug effects | Mitogen-Activated Protein Kinase 8 - genetics | Aortic Diseases - enzymology | Proto-Oncogene Proteins c-akt - metabolism | Aorta - enzymology | Aortic Diseases - pathology | Disease Models, Animal | Receptors, LDL - genetics | Atherosclerosis - pathology | Genetic Predisposition to Disease | Macrophages - pathology | Signal Transduction | Cell Survival | Aorta - drug effects | Mice, Inbred C57BL | Bone Marrow Cells - pathology | Cells, Cultured | PTEN Phosphohydrolase - metabolism | Plaque, Atherosclerotic | Mitogen-Activated Protein Kinase 9 - deficiency | Macrophages - enzymology | Mice, Knockout | Aorta - pathology | Mitogen-Activated Protein Kinase 8 - deficiency | Aortic Diseases - genetics | Phenotype | Animals | Endoplasmic Reticulum Stress | Mitogen-Activated Protein Kinase 9 - antagonists & inhibitors | Macrophages - drug effects | Protein Kinase Inhibitors - pharmacology | Hypercholesterolemia - genetics
Journal Article
PLoS Computational Biology, ISSN 1553-734X, 2014, Volume 10, Issue 2, p. e1003470
Interleukin-1 (IL-1) is a large cytokine family closely related to innate immunity and inflammation. IL-1 proteins are key players in signaling pathways such... 
DATA-BANK | KINASE | BIOCHEMICAL RESEARCH METHODS | MATHEMATICAL & COMPUTATIONAL BIOLOGY | INTERFACES | PROTEIN-PROTEIN INTERACTIONS | RECEPTOR | SCALE | MOLECULAR DOCKING | EXPRESSION | SOMATIC MUTATIONS | BRAIN-TUMORS | Interleukin-1 Receptor Accessory Protein - genetics | MAP Kinase Kinase 7 - genetics | Neoplasms - metabolism | Interleukin-1 - genetics | Interleukin-1 Receptor Accessory Protein - chemistry | Humans | MAP Kinase Kinase 7 - chemistry | Mitogen-Activated Protein Kinase 9 - genetics | Mitogen-Activated Protein Kinase 10 - genetics | MAP Kinase Kinase 7 - metabolism | Interleukin-1 Receptor Accessory Protein - metabolism | Receptors, Interleukin-1 Type I - metabolism | Inflammation - metabolism | MAP Kinase Kinase 4 - metabolism | Neoplasms - genetics | Computer Simulation | Receptors, Interleukin-1 Type I - chemistry | Interleukin-1 - chemistry | Oncogenes | Mitogen-Activated Protein Kinase 9 - chemistry | Interleukin-1 - metabolism | Protein Interaction Maps - immunology | Signal Transduction | Mitogen-Activated Protein Kinase 9 - metabolism | Computational Biology | Models, Molecular | Inflammation - immunology | Mitogen-Activated Protein Kinase 10 - metabolism | Mitogen-Activated Protein Kinase 10 - chemistry | Mutagenesis | Protein Interaction Maps - genetics | Models, Biological | Neoplasms - immunology | Receptors, Interleukin-1 Type I - genetics | Inflammation - genetics | MAP Kinase Kinase 4 - chemistry | MAP Kinase Kinase 4 - genetics | Polymorphism, Single Nucleotide | Mutation | Complications and side effects | Interleukin-1 | Patient outcomes | Physiological aspects | Development and progression | Inflammation | Genetic aspects | Research | Risk factors | Genetic polymorphisms | Apoptosis | Proteins | Cytokines | Disease | Kinases | Cancer
Journal Article
Science, ISSN 0036-8075, 1/2013, Volume 339, Issue 6116, pp. 218 - 222
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2015, Volume 10, Issue 4, p. 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
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 10/2009, Volume 119, Issue 10, pp. 2925 - 2941
ER stress-induced apoptosis is implicated in various pathological conditions, but the mechanisms linking ER stress-mediated signaling to downstream apoptotic... 
ADVANCED ATHEROSCLEROTIC LESIONS | MEDICINE, RESEARCH & EXPERIMENTAL | TARGETED DISRUPTION | INHIBITION PROTECTS | CHOLESTEROL-LOADED MACROPHAGES | CARDIAC RYANODINE RECEPTOR | ENDOPLASMIC-RETICULUM STRESS | C-JUN | CELL-DEATH | MEMBRANE PERMEABILIZATION | PARKINSONS-DISEASE | RNA, Small Interfering - genetics | Calcium - metabolism | Humans | Stress, Physiological | Endoplasmic Reticulum - metabolism | Mitogen-Activated Protein Kinase 9 - genetics | fas Receptor - metabolism | Macrophages, Peritoneal - cytology | Epithelial Cells - physiology | STAT1 Transcription Factor - metabolism | fas Receptor - genetics | Membrane Potential, Mitochondrial - physiology | Epithelial Cells - cytology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Mitogen-Activated Protein Kinase 9 - metabolism | Mice, Inbred C57BL | Cells, Cultured | Mitochondria - metabolism | Cholesterol - metabolism | STAT1 Transcription Factor - genetics | Mice, Knockout | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics | Kidney Tubules - cytology | Animals | Thapsigargin - metabolism | Mice | Apoptosis - physiology | Enzyme Activation | Macrophages, Peritoneal - metabolism | RNA, Small Interfering - metabolism | Mitochondria | Cell physiology | Research | Properties | Observations | Protein kinases | Endoplasmic reticulum | Apoptosis
Journal Article
Molecular Cell, ISSN 1097-2765, 03/2012, Volume 45, Issue 6, pp. 777 - 789
Abnormal inflammatory signaling activation occurs commonly in cancer cells. However, how it is initiated and maintained and its roles in early stages of... 
BREAST-CANCER | PATHWAYS | CELLS | PHOSPHORYLATION | JNK | BIOCHEMISTRY & MOLECULAR BIOLOGY | PROSTATE-CANCER | IN-VIVO | ALPHA | CYTOKINE | NF-KAPPA-B | CELL BIOLOGY | Mitogen-Activated Protein Kinase Kinases - genetics | Epithelial Cells - metabolism | Humans | JNK Mitogen-Activated Protein Kinases - metabolism | MicroRNAs - metabolism | NF-kappa B - metabolism | Mitogen-Activated Protein Kinase 9 - genetics | Transcription Factor RelA - genetics | Heat Shock Transcription Factors | DNA-Binding Proteins - metabolism | Mitogen-Activated Protein Kinase Kinases - metabolism | Inflammation - metabolism | Cell Transformation, Neoplastic - genetics | Estrogen Receptor alpha - metabolism | Female | Chemokine CCL2 - metabolism | JNK Mitogen-Activated Protein Kinases - genetics | Interleukin-6 - metabolism | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Promoter Regions, Genetic | Interleukin-6 - genetics | Breast - cytology | Mitogen-Activated Protein Kinase 9 - metabolism | Chemokine CCL2 - genetics | Epithelial Cells - pathology | Mice, Transgenic | Signal Transduction - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Transcription Factors - metabolism | Animals | NF-kappa B - genetics | Transcription Factor RelA - metabolism | Inflammation - genetics | Mice | Analysis | Tumors
Journal Article
Gastroenterology, ISSN 0016-5085, 2008, Volume 135, Issue 4, pp. 1311 - 1321
Background & Aims: Acetaminophen (APAP) overdose is the most frequent cause of drug-induced liver failure. C-jun N-terminal kinase (JNK) is thought to play a... 
Gastroenterology and Hepatology | JNK ACTIVATION | APOPTOSIS | GAMMA-RADIATION | PROTEIN-KINASE | MAP KINASES | TNF-ALPHA | STRESS | GASTROENTEROLOGY & HEPATOLOGY | ISOLATED MOUSE HEPATOCYTES | CELL-DEATH | INDUCED HEPATOTOXICITY | Drug Overdose - metabolism | Hepatocytes - pathology | JNK Mitogen-Activated Protein Kinases - metabolism | Male | Mitogen-Activated Protein Kinase 9 - genetics | Drug Overdose - pathology | Acetaminophen - poisoning | Mitogen-Activated Protein Kinase 8 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | JNK Mitogen-Activated Protein Kinases - genetics | MAP Kinase Kinase Kinase 5 - metabolism | Chemical and Drug Induced Liver Injury - pathology | Disease Models, Animal | Drug Overdose - physiopathology | MAP Kinase Kinase Kinase 5 - genetics | Mitogen-Activated Protein Kinase 9 - metabolism | Mice, Inbred C57BL | Mitogen-Activated Protein Kinase 8 - metabolism | p38 Mitogen-Activated Protein Kinases - genetics | Chemical and Drug Induced Liver Injury - physiopathology | Mice, Knockout | Gene Expression Regulation, Enzymologic | Animals | Signal Transduction - drug effects | Chemical and Drug Induced Liver Injury - metabolism | Signal Transduction - physiology | Mice | Analgesics, Non-Narcotic - poisoning | Hepatocytes - enzymology | Liver diseases | Protein kinases | Liver | Glutathione | Apoptosis | Index Medicus | Abridged Index Medicus
Journal Article
Journal Article
Gastroenterology, ISSN 0016-5085, 2016, Volume 150, Issue 4, pp. 968 - 981
Background & Aims c-Jun N-terminal kinase (JNK) 1 and JNK2 are expressed in hepatocytes and have overlapping and distinct functions. JNK proteins are activated... 
Gastroenterology and Hepatology | APAP | Gene Regulation | Pharmacologic Treatment | Mouse Model | APOPTOSIS | ACETAMINOPHEN-INDUCED HEPATOTOXICITY | OXIDATIVE STRESS | ACTIVATION | MOUSE HEPATOCYTES | TERMINAL KINASE | SIGNAL-TRANSDUCTION | MITOCHONDRIAL PERMEABILITY TRANSITION | NECROSIS | INHIBITION | GASTROENTEROLOGY & HEPATOLOGY | AMP-Activated Protein Kinases - metabolism | Phosphorylation | Cell Proliferation | Mitogen-Activated Protein Kinase 8 - antagonists & inhibitors | Oxidative Stress | Carbon Tetrachloride | Humans | Middle Aged | Liver Failure, Acute - enzymology | Hepatocytes - pathology | Male | Gene Expression Profiling | Mitogen-Activated Protein Kinase 9 - genetics | Case-Control Studies | Young Adult | Time Factors | Liver Failure, Acute - genetics | Cell Death | Female | Mitogen-Activated Protein Kinase 8 - genetics | Liver Failure, Acute - prevention & control | Chemical and Drug Induced Liver Injury - pathology | Chemical and Drug Induced Liver Injury - enzymology | Hepatocytes - drug effects | Disease Models, Animal | Chemical and Drug Induced Liver Injury - prevention & control | Signal Transduction | Mitogen-Activated Protein Kinase 9 - metabolism | Mice, Inbred C57BL | Mitogen-Activated Protein Kinase 8 - metabolism | Cells, Cultured | Liver Failure, Acute - chemically induced | Chemical and Drug Induced Liver Injury - genetics | Mitogen-Activated Protein Kinase 9 - deficiency | Mice, Knockout | Mitogen-Activated Protein Kinase 8 - deficiency | Animals | Acetaminophen | Liver Failure, Acute - pathology | Mitogen-Activated Protein Kinase 9 - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | Enzyme Activation | Hepatocytes - enzymology | Proteins | Medical colleges | Liver diseases | Liver | Carbon tetrachloride | Physiological aspects | Index Medicus | Abridged Index Medicus | pharmacological treatment | mouse model | gene regulation
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 7/2006, Volume 103, Issue 28, pp. 10741 - 10746
Journal Article
PLoS ONE, ISSN 1932-6203, 10/2013, Volume 8, Issue 10, p. e77300
Injuring mouse corneas with alkali causes myofibroblast expression leading to tissue opacification. However, in transient receptor potential vanilloid 1... 
CELLS | ACTIVATION | POSITIVE FEEDBACK | MAP KINASE | MULTIDISCIPLINARY SCIENCES | TISSUE FIBROSIS | RECEPTOR | OXIDASE EXPRESSION | DIFFERENTIATION | FIBROBLASTS | KERATOCYTES | Corneal Opacity - chemically induced | Reactive Oxygen Species - metabolism | Calcium - metabolism | Humans | Actins - metabolism | Corneal Opacity - metabolism | Mitogen-Activated Protein Kinase 9 - genetics | Actins - genetics | Myofibroblasts - metabolism | TRPV Cation Channels - metabolism | Swine | TRPV Cation Channels - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - genetics | Smad2 Protein - genetics | Mitogen-Activated Protein Kinase 8 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Corneal Injuries | Alkalies | Myofibroblasts - pathology | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Mitogen-Activated Protein Kinase 9 - metabolism | Tissue Culture Techniques | Mitogen-Activated Protein Kinase 8 - metabolism | Gene Expression Regulation | Smad2 Protein - metabolism | p38 Mitogen-Activated Protein Kinases - genetics | Corneal Opacity - genetics | TRPV Cation Channels - genetics | Cornea - metabolism | Transforming Growth Factor beta - pharmacology | Feedback, Physiological | Animals | Transforming Growth Factor beta - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Mice | Transforming Growth Factor beta - metabolism | Mitogen-Activated Protein Kinase 1 - metabolism | Cell culture | Flow cytometry | Oxidative stress | Phosphorylation | Cornea | Reactive oxygen species | Transparency | Smooth muscle | Capsaicin receptors | Activation | Feedback loops | Positive feedback | Calcium influx | Western blotting | Proteins | Transient receptor potential proteins | Transfection | Restoration | Protein folding | Actin | Smad2 protein | Fibroblasts | Growth factors | Phenotypes | Wound healing | Calcium (intracellular) | Muscles | Extracellular signal-regulated kinase | Optometry | siRNA | Gene expression | Capsazepine | Medicine | Cytometry | Gene flow | Calcium ions
Journal Article