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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 | Index Medicus
Journal Article
Journal of the National Cancer Institute, ISSN 0027-8874, 09/2012, Volume 104, Issue 17, pp. 1306 - 1319
Previous studies identified the human nonmetastatic gene 23 (NME1, hereafter Nm23-H1) as the first metastasis suppressor gene. An inverse relationship between... 
SIGNAL-TRANSDUCTION | GREEN FLUORESCENT PROTEIN | IN-VITRO | ONCOLOGY | SUPPRESSOR PROTEINS | CARCINOMA-CELL-LINE | KINASE ALPHA-ISOFORM | PROTEIN-COUPLED RECEPTORS | ADENOCARCINOMA CELLS | TUMOR-GROWTH | DIPHOSPHATE KINASE | Immunohistochemistry | Propionates - pharmacology | Gene Expression Regulation, Enzymologic - drug effects | eIF-2 Kinase - metabolism | Lung Neoplasms - metabolism | Ki-67 Antigen - metabolism | Receptors, Lysophosphatidic Acid - genetics | Mammary Neoplasms, Experimental - metabolism | eIF-2 Kinase - drug effects | NM23 Nucleoside Diphosphate Kinases - metabolism | Lung Neoplasms - secondary | Mammary Neoplasms, Experimental - pathology | NM23 Nucleoside Diphosphate Kinases - drug effects | Female | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Receptors, Lysophosphatidic Acid - antagonists & inhibitors | Liver Neoplasms - secondary | Mammary Neoplasms, Experimental - drug therapy | Liver Neoplasms - prevention & control | RNA, Small Interfering - pharmacology | Random Allocation | Blotting, Western | Isoxazoles - pharmacology | Animals | MAP Kinase Signaling System - drug effects | Analysis of Variance | Lung Neoplasms - prevention & control | Mice, Nude | Liver Neoplasms - metabolism | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Mice, Inbred BALB C | Ki-67 Antigen - drug effects | Animal experimentation | Care and treatment | Usage | Analysis | Physiological aspects | Genetic aspects | Breast cancer | Metastasis | Gene expression | Clinical trials | Index Medicus
Journal Article
Journal of Periodontology, ISSN 0022-3492, 03/2015, Volume 86, Issue 3, pp. 440 - 447
Journal Article
Journal Article
Journal Article
BMC Gastroenterology, ISSN 1471-230X, 02/2016, Volume 16, Issue 1, pp. 25 - 25
Journal Article
The EMBO Journal, ISSN 0261-4189, 01/2004, Volume 23, Issue 1, pp. 169 - 179
Transient phosphorylation of the α‐subunit of translation initiation factor 2 (eIF2α) represses translation and activates select gene expression under diverse... 
protein kinases | translation | signal transduction | reactive oxygen species | preconditioning | Signal transduction | Reactive oxygen species | Translation | Preconditioning | Protein kinases | UNFOLDED-PROTEIN RESPONSE | BIOCHEMISTRY & MOLECULAR BIOLOGY | KINASE | CELL BIOLOGY | PROGRAMMED CELL-DEATH | INDUCED GENE-EXPRESSION | FACTOR 2-ALPHA | GLUTATHIONE DISULFIDE | LINE | OXIDATIVE GLUTAMATE TOXICITY | ENDOPLASMIC-RETICULUM | STRESS | Phosphorylation | Protein Biosynthesis | Reactive Oxygen Species - metabolism | Oxidative Stress | eIF-2 Kinase - metabolism | Activating Transcription Factor 4 | Endoplasmic Reticulum - metabolism | Tacrolimus - analogs & derivatives | eIF-2 Kinase - drug effects | Recombinant Fusion Proteins - metabolism | Glutamates - toxicity | Retroviridae - genetics | Tacrolimus - pharmacology | Eukaryotic Initiation Factor-2 - metabolism | Dimerization | Cytoprotection | Pancreas - enzymology | Endoplasmic Reticulum - enzymology | Protein Structure, Tertiary | Cell Survival - drug effects | Signal Transduction | Enzyme Inhibitors - pharmacology | Gene Expression Regulation | eIF-2 Kinase - chemistry | Animals | Tunicamycin - pharmacology | Thapsigargin - pharmacology | Trans-Activators - metabolism | Mice | Enzyme Activation | Cell Line, Transformed | Cell Transformation, Viral | PERK protein | initiation factor eIF-2 | Index Medicus | PERK, pancreatic endoplasmic reticulum kinase | ATF4, activating transcription factor 4 | eIF2, eukaryotic translation initiation factor-2 | EBP homologous proteins | DCF, dichlorofluorescein | β-ME, β-mercaptoethanol | CHOP, C | GADD34, growth arrest and DNA damage gene 34 | Abbreviations | ISR, integrated stress response
Journal Article
Free Radical Biology and Medicine, ISSN 0891-5849, 2008, Volume 44, Issue 6, pp. 1097 - 1107
Cigarette smoke (CS) generally places severe stress on cells, as reflected by gene expression profiling and pathway analysis, which, among other effects, also... 
ER stress | Oxidative stress | Acrolein | PERK | Cigarette smoke | BIOCHEMISTRY & MOLECULAR BIOLOGY | KAPPA-B | INDUCTION | cigarette smoke | TRANSLATION | acrolein | NRF2 | GLUTATHIONE | DISEASE | ENDOCRINOLOGY & METABOLISM | GENE-EXPRESSION | INDUCED EMPHYSEMA | oxidative stress | Alternative Splicing | Gene Expression - drug effects | eIF-2 Kinase - metabolism | Oxidative Stress - physiology | Molecular Sequence Data | eIF-2 Kinase - drug effects | X-Box Binding Protein 1 | Base Sequence | Endoplasmic Reticulum - drug effects | Nuclear Proteins - drug effects | Nuclear Proteins - genetics | Fibroblasts - metabolism | Cell Survival - drug effects | DNA-Binding Proteins - drug effects | DNA-Binding Proteins - genetics | Reverse Transcriptase Polymerase Chain Reaction | Activating Transcription Factor 4 - drug effects | Regulatory Factor X Transcription Factors | Blotting, Western | Animals | Tobacco Smoke Pollution - adverse effects | Activating Transcription Factor 4 - metabolism | Signal Transduction - drug effects | Fibroblasts - drug effects | Signal Transduction - physiology | Mice | Transcription Factors | Oxidative Stress - drug effects | RNA, Messenger | 3T3 Cells | Phosphates | Lung diseases, Obstructive | Acetylcysteine | Protein biosynthesis | Genetic translation | Surface active agents | Analysis | Nitric oxide | Genetic research | DNA polymerases | Binding proteins | Smoking | Protein binding | Index Medicus
Journal Article
Neurobiology of Disease, ISSN 0969-9961, 2009, Volume 34, Issue 2, pp. 357 - 365
Abstract Maternal inheritance of a pathogenic point mutation within complex I of the mitochondrial genome causes Leber's hereditary optic neuropathy (LHON),... 
Neurology | LHON | Oligodendroglia | Mitochondria | Complex I | Integrated stress response | Retrograde signaling | DNA MUTATION | INDUCED APOPTOSIS | MAMMALIAN-CELLS | NEUROSCIENCES | UNFOLDED PROTEIN RESPONSE | COMPLEX-I | NADH DEHYDROGENASE | GENE-EXPRESSION | WHITE-MATTER DISEASE | CELL-CYCLE | HEREDITARY OPTIC NEUROPATHY | Oligodendroglia - metabolism | Optic Nerve - pathology | eIF-2 Kinase - metabolism | Humans | Optic Atrophy, Hereditary, Leber - genetics | Adenosine Triphosphate - biosynthesis | eIF-2 Kinase - drug effects | Transcription Factors - drug effects | Dose-Response Relationship, Drug | Transcription Factor CHOP - drug effects | Mitogen-Activated Protein Kinase 8 - drug effects | Cell Respiration - genetics | Mitochondria - genetics | Optic Atrophy, Hereditary, Leber - metabolism | Electron Transport Complex I - genetics | Cell Respiration - drug effects | Optic Nerve - physiopathology | Optic Atrophy, Hereditary, Leber - physiopathology | Cell Line | Stress, Physiological - genetics | Mitogen-Activated Protein Kinase 8 - metabolism | Mitochondria - metabolism | Enzyme Activation - drug effects | Activating Transcription Factor 4 - drug effects | Uncoupling Agents - toxicity | Oligodendroglia - pathology | Transcription Factors - metabolism | Activating Transcription Factor 4 - metabolism | Cell Line, Tumor | Cell Proliferation - drug effects | Enzyme Activation - genetics | Transcription Factor CHOP - metabolism | Optic Nerve - metabolism | Analysis | Mitochondrial DNA | Index Medicus
Journal Article
BMC Microbiology, ISSN 1471-2180, 08/2017, Volume 17, Issue 1, pp. 187 - 187
Background: The bronchial epithelium serves as the first defendant line of host against respiratory inhaled pathogens, mainly through releasing chemokines... 
PepO | BEAS-2B | Il-8 | IP-10 | IMMUNE-RESPONSE | DEFENSE | INNATE | NEUTROPHILS | MICROBIOLOGY | FACTOR-KAPPA-B | COLONIZATION | PNEUMOLYSIN | INTERLEUKIN-8 | RESISTANCE | PNEUMOCOCCAL PNEUMONIA | Interleukin-8 - genetics | Phosphorylation | Epithelial Cells - metabolism | Epithelial Cells - drug effects | Humans | eIF-2 Kinase - drug effects | Phosphatidylinositol 3-Kinases | Streptococcus pneumoniae - pathogenicity | Time Factors | Streptococcus pneumoniae - metabolism | Bronchi - metabolism | Transcription, Genetic | p38 Mitogen-Activated Protein Kinases - metabolism | Interleukin-8 - metabolism | Recombinant Proteins - metabolism | Cell Line | Cytokines - metabolism | Metalloendopeptidases - administration & dosage | Toll-Like Receptor 2 - metabolism | Toll-Like Receptor 4 - metabolism | Virulence Factors | Bacterial Proteins - administration & dosage | Gene Expression Regulation, Enzymologic | Bacterial Proteins - pharmacology | Signal Transduction - drug effects | Chemokine CXCL10 - genetics | Metalloendopeptidases - pharmacology | NF-KappaB Inhibitor alpha - metabolism | Mitogen-Activated Protein Kinase Kinases - drug effects | Chemokine CXCL10 - metabolism | Polysaccharides | Pneumonia | Interleukins | Bacterial pneumonia | B cells | Biological response modifiers | Streptococcus pneumoniae | Cell culture | Pathogenesis | Epithelial cells | Virulence | Interleukin | AKT protein | Kinases | Recruitment | Streptococcus infections | Proteins | Virulence factors | Lymphocytes | Toll-like receptors | IP-10 protein | Interleukin 8 | Surface protein A | Saccharides | Enzymes | Pathogens | Cytokines | Incubation | Dendritic cells | Peptidoglycans | Neutrophils | MAP kinase | Pharmacology | Inflammation | Protein A | PspA protein | TLR4 protein | Epithelium | Chromatography | 1-Phosphatidylinositol 3-kinase | Studies | Pneumolysin | Streptococcus | Inhibitors | TLR2 protein | Endopeptidase | Ligands | Interferon | Chemokines | Index Medicus
Journal Article