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Blood, ISSN 0006-4971, 2016, Volume 127, Issue 14, pp. 1780 - 1789
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 08/2014, Volume 289, Issue 33, pp. 23246 - 23255
Metformin, a well known antidiabetic agent that improves peripheral insulin sensitivity, also elicits anti-inflammatory actions, but its mechanism is unclear.... 
DIABETES-MELLITUS | RESPIRATORY-CHAIN | 5-AMINOIMIDAZOLE-4-CARBOXAMIDE RIBOSIDE | MECHANISM | NITRIC-OXIDE SYNTHASE | PROTEIN-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENE-EXPRESSION | FACTOR-KAPPA-B | VASCULAR ENDOTHELIAL-CELLS | NEGATIVE REGULATOR | Inflammation - chemically induced | Inflammation - pathology | AMP-Activated Protein Kinases - metabolism | Endotoxemia - genetics | Tumor Necrosis Factor-alpha - genetics | Male | Endotoxemia - pathology | Extracellular Signal-Regulated MAP Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - genetics | Gene Knockdown Techniques | Inflammation - metabolism | Phosphorylation - genetics | Phosphorylation - drug effects | Activating Transcription Factor 3 - genetics | Cell Line | Lipopolysaccharides - toxicity | Interleukin-6 - genetics | Macrophages - pathology | Anti-Inflammatory Agents - pharmacology | Metformin - pharmacology | Activating Transcription Factor 3 - metabolism | Hypoglycemic Agents - pharmacology | Macrophages - metabolism | Animals | Interleukin-6 - biosynthesis | Mice, Obese | Mice | Endotoxemia - blood | Endotoxemia - metabolism | Tumor Necrosis Factor-alpha - biosynthesis | AMP-Activated Protein Kinases - genetics | Index Medicus | Interleukin 6 (IL-6) | ATF-3 | Signal Transduction | Tumor Necrosis Factor (TNF) | Inflammation | Metformin | Lipopolysaccharide (LPS) | Macrophage
Journal Article
Cancer Cell, ISSN 1535-6108, 04/2015, Volume 27, Issue 4, pp. 516 - 532
Journal Article
Circulation, ISSN 0009-7322, 04/2017, Volume 135, Issue 21, pp. 2041 - 2057
BACKGROUND—Hypertensive ventricular remodeling is a common cause of heart failure. However, the molecular mechanisms regulating ventricular remodeling remain... 
Heart failure | Fibroblast | P38 mitogenactivated protein kinases | Activating transcription factor 3 | FIBROSIS | heart failure | CARDIAC & CARDIOVASCULAR SYSTEMS | CARDIOMYOPATHY | p38 mitogen-activated protein kinases | BETA | HYPERTROPHY | fibroblast | INHIBITION | INFLAMMATION | DISEASE | GENE-EXPRESSION | PERIPHERAL VASCULAR DISEASE | CELL | activating transcription factor 3 | ATF3 | Fibroblasts - enzymology | Hypertrophy, Left Ventricular - enzymology | Ventricular Function, Left | Heart Failure - enzymology | Humans | Heart Failure - physiopathology | Male | MAP Kinase Kinase 3 - genetics | Heart Failure - prevention & control | Ventricular Remodeling | Time Factors | Hypertension - chemically induced | p38 Mitogen-Activated Protein Kinases - metabolism | Acetylation | Angiotensin II | Binding Sites | Heart Failure - etiology | Activating Transcription Factor 3 - genetics | Disease Models, Animal | Promoter Regions, Genetic | Genetic Predisposition to Disease | Signal Transduction | Hypertrophy, Left Ventricular - etiology | Hypertrophy, Left Ventricular - prevention & control | Activating Transcription Factor 3 - deficiency | Cells, Cultured | Myocardium - pathology | Fibroblasts - pathology | Activating Transcription Factor 3 - metabolism | MAP Kinase Kinase 3 - metabolism | Mice, Knockout | Myocardium - enzymology | Phenotype | Animals | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Fibrosis | Protein Kinase Inhibitors - pharmacology | Histones - metabolism | Hypertrophy, Left Ventricular - physiopathology | Transforming Growth Factor beta - metabolism | Histone Deacetylase 1 - metabolism | Index Medicus | Abridged Index Medicus | p38 MAPK | cardiac fibroblast
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 09/2014, Volume 229, Issue 9, pp. 1202 - 1211
Transcriptional repressor activating transcription factor 3 (ATF3) is induced by various stress stimuli, including inflammation-induced renal injury. In... 
BIOMARKERS | ACUTE KIDNEY INJURY | ACTIVATION | PHYSIOLOGY | PROTEIN | MESSENGER-RNA | TUBULAR INJURY | ENDOTHELIAL-CELLS | DISEASE | PROMOTER | IDENTIFICATION | CELL BIOLOGY | Kidney - blood supply | Kidney - pathology | Humans | Middle Aged | Male | RNA, Messenger - metabolism | Kidney - metabolism | RNA Interference | Time Factors | Exosomes - immunology | Aged, 80 and over | Transcription, Genetic | Acute Kidney Injury - immunology | Binding Sites | Activating Transcription Factor 3 - genetics | Disease Models, Animal | Signal Transduction | Acute Kidney Injury - pathology | Down-Regulation | Activating Transcription Factor 3 - deficiency | Rats | Mice, Knockout | Macrophages - metabolism | Activating Transcription Factor 3 - urine | Mice | Acute Kidney Injury - metabolism | Exosomes - metabolism | Acute Kidney Injury - urine | Epithelial Cells - metabolism | Kidney - immunology | Acute Kidney Injury - genetics | Transfection | Reperfusion Injury - urine | Inflammation Mediators - metabolism | Adult | Female | Chemokine CCL2 - metabolism | Reperfusion Injury - genetics | Reperfusion Injury - metabolism | Macrophages - immunology | Cell Line | Promoter Regions, Genetic | Reperfusion Injury - pathology | Mice, Inbred C57BL | Chemokine CCL2 - genetics | Activating Transcription Factor 3 - metabolism | Animals | Epithelial Cells - immunology | Reperfusion Injury - immunology | Aged | Genetic aspects | Genetic transcription | Ischemia | RNA | Analysis | Genes | Index Medicus
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 12/2017, Volume 232, Issue 12, pp. 3727 - 3734
Excessive inflammatory responses are critical in the pathogenesis of acute lung injury (ALI). Activating transcription factor 3 (ATF3) is a stress‐induced... 
inflammation | acute lung injury | RRID | ATF3 | TL1A | RHEUMATOID-ARTHRITIS | PHYSIOLOGY | TNF-LIKE LIGAND | MACROPHAGES | MONOCYTES | T-CELL | CELL BIOLOGY | COSTIMULATOR | Capillary Permeability | Oligonucleotide Array Sequence Analysis | Acute Lung Injury - genetics | Lipopolysaccharides | Transfection | RNA Interference | Time Factors | Acute Lung Injury - prevention & control | Inflammation Mediators - metabolism | Acute Lung Injury - metabolism | Lung - metabolism | Tumor Necrosis Factor Ligand Superfamily Member 15 - genetics | Cytokines - genetics | Activating Transcription Factor 3 - genetics | Disease Models, Animal | Genetic Predisposition to Disease | Lung - pathology | Cytokines - metabolism | Signal Transduction | Down-Regulation | Mice, Inbred C57BL | Activating Transcription Factor 3 - deficiency | Gene Expression Profiling - methods | Tumor Necrosis Factor Ligand Superfamily Member 15 - metabolism | Activating Transcription Factor 3 - metabolism | Mice, Knockout | Macrophages - metabolism | Phenotype | Animals | Acute Lung Injury - chemically induced | RAW 264.7 Cells | Mice | Bronchoalveolar Lavage Fluid - chemistry | Lung - blood supply | Acute respiratory distress syndrome | Genetic research | Gene expression | Mitogens | Analysis | Transcription factors | Pathogenesis | Lung | Activating transcription factor 3 | Stimulation | siRNA | Inflammation | Injection | Tissues | Macrophages | Interleukin 6 | Tumor necrosis factor | Rodents | Interleukin 1 | Inhibition | Plates | Peritoneum | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 04/2018, Volume 556, Issue 7702, pp. 501 - 504
Journal Article
Nature, ISSN 0028-0836, 05/2010, Volume 465, Issue 7296, pp. 368 - 372
Calcineurin inhibitors such as cyclosporin A (CsA) are the mainstay of immunosuppressive treatment for organ transplant recipients. Squamous cell carcinoma... 
STEM-CELLS | INHIBITOR DSCR1 | TUMOR SUPPRESSION | MULTIDISCIPLINARY SCIENCES | GROWTH | TRANSFORMED PHENOTYPE | C-MYC | PROLIFERATION | DIFFERENTIATION | CELLULAR SENESCENCE | CARCINOMA | Neoplasm Transplantation | Cell Proliferation | Cyclosporine - pharmacology | Carcinoma, Squamous Cell - metabolism | Carcinoma, Squamous Cell - pathology | Humans | Carcinoma, Squamous Cell - chemically induced | Gene Expression Regulation, Neoplastic | Gene Knockdown Techniques | Calcineurin Inhibitors | Calcineurin - genetics | Cell Transformation, Neoplastic - genetics | Cellular Senescence | Skin Neoplasms - pathology | Signal Transduction | NFATC Transcription Factors - metabolism | Cells, Cultured | Tumor Suppressor Protein p53 - metabolism | Skin Neoplasms - chemically induced | Mice, SCID | Activating Transcription Factor 3 - metabolism | Cell Transformation, Neoplastic - metabolism | Skin Neoplasms - metabolism | Keratinocytes - pathology | Animals | Calcineurin - deficiency | Keratinocytes - metabolism | Cell Line, Tumor | Mice, Inbred NOD | Mice | NFATC Transcription Factors - deficiency | NFATC Transcription Factors - antagonists & inhibitors | Calcineurin - metabolism | NFATC Transcription Factors - genetics | Squamous cell carcinoma | Transcription factors | Calcineurin | Physiological aspects | Diagnosis | Research | Risk factors | Mutation | Cysts | Genes | Binding sites | Cancer | Index Medicus
Journal Article