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American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2016, Volume 311, Issue 4, pp. H871 - H880
We previously reported that endoplasmic reticulum (ER) stress is induced in the subfornical organ (SFO) and the hypothalamic paraventricular nucleus (PVN) of... 
Heart failure | Brain | Sympathetic activity | Hypothalamic paraventricular nucleus | Mitogen-activated protein kinase | Subfornical organ | Endoplasmic reticulum stress | heart failure | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | INDUCED PHOSPHORYLATION | MYOCARDIAL-INFARCTION | ER STRESS | subfornical organ | KINASE | RATS | sympathetic activity | KAPPA-B | brain | endoplasmic reticulum stress | hypothalamic paraventricular nucleus | mitogen-activated protein kinase | UNFOLDED PROTEIN RESPONSE | PERIPHERAL VASCULAR DISEASE | UP-REGULATION | Cholagogues and Choleretics - pharmacology | Tumor Necrosis Factor-alpha - genetics | Heart Failure - physiopathology | Male | NF-KappaB Inhibitor alpha - genetics | Peptidyl-Dipeptidase A - drug effects | Interleukin-1beta - genetics | Sympathetic Nervous System - physiopathology | RNA, Messenger - metabolism | Activating Transcription Factor 6 - genetics | Subfornical Organ - drug effects | Brain - metabolism | Heat-Shock Proteins - genetics | Inflammation - metabolism | Receptor, Angiotensin, Type 1 - genetics | Cyclooxygenase 2 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Real-Time Polymerase Chain Reaction | Echocardiography | Signal Transduction | Rats | Cyclooxygenase 2 - drug effects | Heart Failure - metabolism | Rats, Sprague-Dawley | Blotting, Western | Brain - drug effects | Tumor Necrosis Factor-alpha - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Endoplasmic Reticulum Stress | Paraventricular Hypothalamic Nucleus - metabolism | Infusions, Intraventricular | Mitogen-Activated Protein Kinases - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Interleukin-1beta - drug effects | Sympathetic Nervous System - drug effects | Mitogen-Activated Protein Kinase 1 - drug effects | X-Box Binding Protein 1 - drug effects | Sympathetic Nervous System - metabolism | Transcription Factor RelA - genetics | Activating Transcription Factor 6 - drug effects | Mitogen-Activated Protein Kinase 3 - drug effects | Taurochenodeoxycholic Acid - pharmacology | Peptidyl-Dipeptidase A - genetics | Renin-Angiotensin System | Receptor, Angiotensin, Type 1 - drug effects | RNA, Messenger - drug effects | Subfornical Organ - metabolism | Heat-Shock Proteins - drug effects | Activating Transcription Factor 4 - genetics | Activating Transcription Factor 4 - drug effects | NF-KappaB Inhibitor alpha - drug effects | Paraventricular Hypothalamic Nucleus - drug effects | p38 Mitogen-Activated Protein Kinases - drug effects | Animals | Transcription Factor RelA - drug effects | X-Box Binding Protein 1 - genetics | Mitogen-Activated Protein Kinases - metabolism | Physiological aspects | Cellular signal transduction | Endoplasmic reticulum | Health aspects | Mitogen-activated protein kinases | Cardiovascular Neurohormonal Regulation
Journal Article
Journal Article
Cardiovascular Diabetology, ISSN 1475-2840, 11/2013, Volume 12, Issue 1, pp. 158 - 158
Background: Endoplasmic reticulum (ER) stress is considered one of the mechanisms contributing to reactive oxygen species (ROS)-mediated cell apoptosis. In... 
Diabetic cardiomyopathy | Oxidative stress | Apoptosis | Endoplasmic reticulum stress | MITOCHONDRIAL OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | ER STRESS | PREVENTION | SUPPRESSION | RAT MODEL | MYOCARDIAL APOPTOSIS | CELL-DEATH | HEART | ENDOCRINOLOGY & METABOLISM | MICE | CONTRIBUTES | Free Radical Scavengers - pharmacology | Diabetic Cardiomyopathies - metabolism | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | eIF-2 Kinase - metabolism | eIF-2 Kinase - drug effects | Activating Transcription Factor 6 - genetics | Activating Transcription Factor 6 - drug effects | Gene Knockdown Techniques | Membrane Proteins - metabolism | Diabetes Mellitus, Experimental - metabolism | Protein-Serine-Threonine Kinases - metabolism | Disease Models, Animal | Endoplasmic Reticulum Stress - drug effects | Membrane Proteins - genetics | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Rats | Rats, Sprague-Dawley | Activating Transcription Factor 6 - metabolism | Animals | Myocytes, Cardiac - drug effects | Signal Transduction - drug effects | Acetylcysteine - pharmacology | Protein-Serine-Threonine Kinases - drug effects | Glucose - metabolism | Membrane Proteins - drug effects | Myocytes, Cardiac - metabolism | Signal Transduction - physiology | Apoptosis - physiology | Endoplasmic Reticulum Stress - physiology | Studies | Kinases | Rodents | Animal models
Journal Article
Journal Article
Journal Article
Journal of Periodontology, ISSN 0022-3492, 03/2015, Volume 86, Issue 3, pp. 440 - 447
Journal Article
Cellular and Molecular Neurobiology, ISSN 0272-4340, 3/2009, Volume 29, Issue 2, pp. 181 - 192
Simvastatin is a cholesterol-lowering agent whose functional significance and neuroprotective mechanism in ischemic brain injury is not yet solved. The purpose... 
Neuroprotective effect | Neurosciences | Biomedicine | Animal Anatomy / Morphology / Histology | Statins | Unfolded protein response | Global brain ischemia | REDUCTASE INHIBITORS | OXIDATIVE STRESS | NITRIC-OXIDE SYNTHASE | TIME-COURSE | NEUROSCIENCES | NEURONAL DAMAGE | CELL BIOLOGY | MESSENGER-RNA | ISCHEMIC BRAIN-INJURY | CEREBRAL-ISCHEMIA | TRANSCRIPTION FACTOR | Molecular Chaperones - metabolism | Rats, Wistar | Oxidative Stress - physiology | Reperfusion Injury - drug therapy | Endoplasmic Reticulum - metabolism | Male | Hypoxia-Ischemia, Brain - genetics | RNA, Messenger - metabolism | Simvastatin - pharmacology | Activating Transcription Factor 6 - genetics | X-Box Binding Protein 1 | Activating Transcription Factor 6 - drug effects | Transcription Factors - drug effects | DNA-Binding Proteins - metabolism | Heat-Shock Proteins - genetics | Neuroprotective Agents - pharmacology | Time Factors | Protein Folding - drug effects | Endoplasmic Reticulum - drug effects | Up-Regulation - physiology | Molecular Chaperones - drug effects | Reperfusion Injury - genetics | Reperfusion Injury - metabolism | Hypoxia-Ischemia, Brain - metabolism | RNA, Messenger - drug effects | Endoplasmic Reticulum - genetics | Heat-Shock Proteins - drug effects | Heat-Shock Proteins - metabolism | DNA-Binding Proteins - drug effects | Hypoxia-Ischemia, Brain - drug therapy | Molecular Chaperones - genetics | Gene Expression Regulation - physiology | Rats | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Regulatory Factor X Transcription Factors | Gene Expression Regulation - drug effects | Transcription Factors - metabolism | Up-Regulation - drug effects | Activating Transcription Factor 6 - metabolism | Animals | Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology | Oxidative Stress - drug effects | Proteins | Animal experimentation | Brain | Messenger RNA | Ischemia | Simvastatin | Universities and colleges | Injuries
Journal Article
Respiratory Research, ISSN 1465-9921, 12/2013, Volume 14, Issue 1, pp. 141 - 141
Journal Article
Journal Article
Nature Immunology, ISSN 1529-2908, 05/2010, Volume 11, Issue 5, pp. 411 - 418
Sensors of pathogens, such as Toll-like receptors (TLRs), detect microbes to activate transcriptional programs that orchestrate adaptive responses to specific... 
UNFOLDED PROTEIN RESPONSE | PATHWAY | ER STRESS | HOST-DEFENSE | ENDOPLASMIC-RETICULUM STRESS | FRANCISELLA-TULARENSIS INFECTION | IMMUNOLOGY | LIVE VACCINE STRAIN | INFLAMMATORY RESPONSE | NEGATIVE REGULATOR | SYSTEMS BIOLOGY | RNA, Small Interfering - genetics | Endoribonucleases - genetics | Tularemia - metabolism | Toll-Like Receptor 2 - genetics | Membrane Glycoproteins - metabolism | Lipopeptides - pharmacology | Transcriptional Activation - drug effects | NADPH Oxidases - metabolism | Tularemia - genetics | Protein Splicing - genetics | Transcriptional Activation - immunology | X-Box Binding Protein 1 | Protein Splicing - drug effects | NADPH Oxidases - genetics | Stress, Physiological - drug effects | TNF Receptor-Associated Factor 6 - genetics | Transcription Factor CHOP - biosynthesis | Transcription Factors - immunology | Cytokines - genetics | Protein-Serine-Threonine Kinases - metabolism | DNA-Binding Proteins - immunology | Endoribonucleases - metabolism | Macrophages - pathology | Stress, Physiological - genetics | Myeloid Differentiation Factor 88 - genetics | Toll-Like Receptor 4 - genetics | Signal Transduction - genetics | Toll-Like Receptor 4 - immunology | Toll-Like Receptor 2 - metabolism | Toll-Like Receptor 4 - metabolism | Mice, Knockout | Macrophages - metabolism | Signal Transduction - drug effects | Tunicamycin - pharmacology | Lipopolysaccharides - pharmacology | Toll-Like Receptor 2 - immunology | Mice | Stress, Physiological - immunology | Endoribonucleases - immunology | Transcription Factor CHOP - genetics | NADPH Oxidases - immunology | DNA-Binding Proteins - metabolism | Signal Transduction - immunology | Macrophages - virology | Mice, Mutant Strains | Tularemia - immunology | Membrane Glycoproteins - immunology | Macrophages - immunology | Cytokines - immunology | Cell Line | Francisella tularensis - immunology | Protein Splicing - immunology | Protein-Serine-Threonine Kinases - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Immunity, Innate | NADPH Oxidase 2 | Regulatory Factor X Transcription Factors | Mice, Inbred C3H | Membrane Glycoproteins - genetics | Transcription Factors - metabolism | Animals | TNF Receptor-Associated Factor 6 - metabolism | Macrophages - drug effects | Protein-Serine-Threonine Kinases - immunology | Francisella tularensis - pathogenicity | Myeloid Differentiation Factor 88 - metabolism | Cytokines - biosynthesis | Cell receptors | Transcription factors | Immune response | Physiological aspects | Genetic aspects | Research | Health aspects | Francisella tularensis
Journal Article
by Zhang, Y and Lei, CQ and Hu, YH and Xia, T and Li, M and Zhong, B and Shu, HB
JOURNAL OF BIOLOGICAL CHEMISTRY, ISSN 0021-9258, 05/2014, Volume 289, Issue 18, pp. 12876 - 12885
Journal Article
PLoS ONE, ISSN 1932-6203, 05/2014, Volume 9, Issue 5, p. e97880
The neurotoxin 6-hydroxydopamine (6-OHDA), which causes transcriptional changes associated with oxidative and proteotoxic stress, has been widely used to... 
OXIDATIVE STRESS | UNFOLDED PROTEIN RESPONSE | HEME OXYGENASE-1 EXPRESSION | LIPID-PEROXIDATION | ER STRESS | MULTIDISCIPLINARY SCIENCES | DNA-DAMAGE | GENE-EXPRESSION | ENDOPLASMIC-RETICULUM STRESS | NERVE GROWTH-FACTOR | PARKINSONS-DISEASE | Transcription Factor CHOP - genetics | Transcription, Genetic - drug effects | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Transcriptional Activation - drug effects | Apoptosis - genetics | Activating Transcription Factor 6 - genetics | PC12 Cells | Heat-Shock Proteins - genetics | Oxidopamine - pharmacology | Stress, Physiological - drug effects | Cell Survival - drug effects | Stress, Physiological - genetics | RNA, Messenger - genetics | Tumor Suppressor Protein p53 - metabolism | Activating Transcription Factor 4 - genetics | Rats | Luteolin - pharmacology | Gene Expression Regulation - drug effects | Activating Transcription Factor 6 - metabolism | Animals | Activating Transcription Factor 4 - metabolism | Signal Transduction - drug effects | Cell Cycle Checkpoints - drug effects | NF-E2-Related Factor 2 - metabolism | Transcription Factor CHOP - metabolism | Antioxidants | Genetic aspects | Genetic transcription | RNA | Tumor proteins | Analysis | Neuroprotection | Cell culture | Oxidative stress | Biotechnology | Reactive oxygen species | Transcription | Toxicity | p53 Protein | Science | Cytotoxicity | Kinases | Caspase-3 | Proteins | Pathways | Protein folding | Rodents | Cell cycle | Stress response | Deoxyribonucleic acid--DNA | Stresses | Enzymes | Neurons | 6-Hydroxydopamine | GADD34 protein | Caspase | Inflammation | Gene expression | Pharmacy | Pheochromocytoma cells | Endoplasmic reticulum | Cellular stress response | Apoptosis | Deoxyribonucleic acid | DNA
Journal Article