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Developmental Cell, ISSN 1534-5807, 03/2017, Volume 40, Issue 6, pp. 583 - 594.e6
Mitochondrial fission mediated by the GTPase dynamin-related protein 1 (Drp1) is an attractive drug target in numerous maladies that range from heart disease... 
succinate | bioenergetics | mitochondria | fission | neuron | reverse electron transfer | respiration | superoxide | brain | fragmentation | ISCHEMIA-REPERFUSION INJURY | BRAIN MITOCHONDRIA | LIFE-SPAN | CELLS | ROS | DYNAMIN-RELATED PROTEIN-1 | DEVELOPMENTAL BIOLOGY | RAT-BRAIN | FISSION | DIVISION | DAMAGE | CELL BIOLOGY | Dynamins - metabolism | Reactive Oxygen Species - metabolism | Microtubule-Associated Proteins - metabolism | Humans | Cercopithecus aethiops | Saccharomyces cerevisiae - drug effects | GTP Phosphohydrolases - antagonists & inhibitors | Electron Transport Complex I - metabolism | Fibroblasts - ultrastructure | Saccharomyces cerevisiae - metabolism | Mitochondrial Proteins - metabolism | Cell Respiration - drug effects | Oxidation-Reduction - drug effects | Neurons - metabolism | NAD - metabolism | Quinazolinones - pharmacology | Fibroblasts - metabolism | Dynamins - antagonists & inhibitors | Electron Transport Complex I - antagonists & inhibitors | Mitochondrial Proteins - antagonists & inhibitors | Mitochondria - metabolism | Microtubule-Associated Proteins - antagonists & inhibitors | Mitochondria - drug effects | Rats, Sprague-Dawley | Mice, Knockout | Animals | GTP Phosphohydrolases - metabolism | Oxygen Consumption - drug effects | Saccharomyces cerevisiae Proteins - metabolism | Mice | COS Cells | Brain | Medical colleges | Nervous system diseases | Heart diseases | Injuries | Biomedical engineering | Neurons | Superoxide
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 07/2017, Volume 292, Issue 28, pp. 11727 - 11739
The mitochondrial network is a major site of ATP production through the coupled integration of the electron transport chain (ETC) with oxidative... 
SUBCHRONIC TOXICITY | MAGNOLIA PLANT | ACTIVATION | MEK INHIBITION | CANCER CELLS | HONOKIOL | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | RESISTANCE | BRAF | VEMURAFENIB | CDC2 Protein Kinase | Mitochondria - enzymology | Cyclin-Dependent Kinases - metabolism | Reactive Oxygen Species - metabolism | Uncoupling Agents - pharmacology | Apoptosis - drug effects | Humans | Neoplasm Proteins - antagonists & inhibitors | G1 Phase - drug effects | Electron Transport Complex II - antagonists & inhibitors | Membrane Potential, Mitochondrial - drug effects | Neoplasm Proteins - metabolism | Electron Transport Complex I - metabolism | Lignans - pharmacology | Reactive Oxygen Species - agonists | Oxidative Phosphorylation - drug effects | Adenosine Triphosphate - antagonists & inhibitors | Biphenyl Compounds - pharmacology | Protein Processing, Post-Translational - drug effects | Adenosine Triphosphate - metabolism | Electron Transport Chain Complex Proteins - antagonists & inhibitors | Cyclin-Dependent Kinases - antagonists & inhibitors | Phosphorylation - drug effects | Cyclin-Dependent Kinase 2 - metabolism | Electron Transport Complex I - antagonists & inhibitors | Mitochondria - drug effects | MAP Kinase Signaling System - drug effects | Electron Transport Complex II - metabolism | Electron Transport Chain Complex Proteins - metabolism | Cell Line, Tumor | Cyclin-Dependent Kinase 2 - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | Antineoplastic Agents, Phytogenic - pharmacology | mitochondrial respiratory chain complex | targeted therapy | mitochondria | apoptosis | respiration | oncogene | Cell Biology | mitochondrial dynamics
Journal Article
Biochemical Journal, ISSN 0264-6021, 09/2014, Volume 462, Issue 3, pp. 475 - 487
The biguanide metformin is widely prescribed for Type II diabetes and has anti-neoplastic activity in laboratory models. Despite evidence that inhibition of... 
ATP synthase | Complex I | Biguanide | Metformin | Reactive oxygen species (ROS) | Nadh:quinone oxidoreductase | CELLS | FLAVIN | ACTIVATED PROTEIN-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | NADH:quinone oxidoreductase | biguanide | metformin | reactive oxygen species (ROS) | RAT-LIVER MITOCHONDRIA | HEART | NADH | INHIBITION | METABOLISM | OXIDOREDUCTASE COMPLEX-I | PURIFICATION | complex I | Biguanides - pharmacology | Triazines - pharmacology | Electron Transport Complex I - antagonists & inhibitors | Metformin - therapeutic use | Biguanides - therapeutic use | Humans | Metformin - pharmacology | Rats | Plasmodium - drug effects | Mitochondria, Heart - drug effects | Electron Transport Complex I - drug effects | Mitochondrial Proton-Translocating ATPases - metabolism | Antimalarials - pharmacology | Hep G2 Cells | Mitochondria, Liver - drug effects | Oxidative Phosphorylation - drug effects | Animals | Reperfusion Injury - prevention & control | Cattle | Antineoplastic Agents - pharmacology | Diabetes Mellitus, Type 2 - drug therapy | Mitochondrial Proton-Translocating ATPases - antagonists & inhibitors | Proguanil - pharmacology | SMP, submitochondrial particle | HAR, hexaammineruthenium(III) | OCR, oxygen consumption rate | AMPK, AMP-activated protein kinase | DMEM, Dulbecco’s modified Eagle’s medium | ECAR, extracellular acidification rate | FeCN, ferricyanide | ROS, reactive oxygen species | OCT1, organic cation transporter 1
Journal Article
Journal Article
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 5, p. e20151
We evaluated the mechanism of capsaicin-mediated ROS generation in pancreatic cancer cells. The generation of ROS was about 4-6 fold more as compared to... 
CHILI | IN-VITRO | ACTIVATION | GASTRIC-CANCER | MULTIDISCIPLINARY SCIENCES | PEPPER | CYCLE ARREST | GENERATION | DEATH | INDUCTION | BENZYL ISOTHIOCYANATE | Mitochondria - enzymology | Electron Transport Complex III - metabolism | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Capsaicin - pharmacology | Antioxidants - metabolism | Humans | Glutathione Disulfide - metabolism | Membrane Potential, Mitochondrial - drug effects | Electron Transport Complex I - metabolism | Adenosine Triphosphate - metabolism | Oxidation-Reduction - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Homeostasis - drug effects | Superoxide Dismutase - metabolism | Glutathione Peroxidase - metabolism | Electron Transport Complex I - antagonists & inhibitors | Pancreatic Neoplasms - pathology | Mitochondria - metabolism | Antioxidants - pharmacology | Mitochondria - drug effects | Catalase - metabolism | Animals | Electron Transport Complex III - antagonists & inhibitors | Lipid Metabolism - drug effects | Cell Line, Tumor | Mice | Capsaicin - antagonists & inhibitors | Oxidative Stress - drug effects | Evaluation | Enzymes | Capsaicin | Mitochondrial DNA | Cytochrome c | Antioxidants | Membrane lipids | Pancreatic cancer | Cancer cells | Phenols | Comparative analysis | Electron transport | Apoptosis | Cytochrome | Health sciences | Oxidative stress | Phosphorylation | Biology | Kinases | Caspase-3 | Cancer therapies | Ovarian cancer | Electron transport chain | Mitochondria | Transfection | Enzymatic activity | Catalase | Rodents | Cell cycle | Oxidation | Peroxidase | Membrane potential | Deoxyribonucleic acid--DNA | Glutathione | Glutathione peroxidase | Caspase | Studies | Overexpression | Medical prognosis | Pharmacy | Caspase-9 | Cardiolipin | Disruption | Prostate | Tumors | Cancer | Deoxyribonucleic acid | DNA
Journal Article
Journal of Immunology, ISSN 0022-1767, 05/2010, Volume 184, Issue 9, pp. 4827 - 4841
This article shows that T cell activation-induced expression of the cytokines IL-2 and -4 is determined by an oxidative signal originating from mitochondrial... 
INTERLEUKIN-2 | ATOPIC-DERMATITIS | COMPLEX-I | REDOX REGULATION | GENE-EXPRESSION | RESPIRATORY INHIBITORS | HYDROGEN-PEROXIDE | DOPAMINERGIC-NEURONS | IMMUNOLOGY | ROTENONE INHIBITION | LYMPHOCYTE-ACTIVATION | DNA, Mitochondrial - antagonists & inhibitors | Mitochondria - enzymology | NADH Dehydrogenase - antagonists & inhibitors | Dermatitis, Atopic - genetics | Reactive Oxygen Species - metabolism | T-Lymphocytes - enzymology | Dermatitis, Atopic - enzymology | Electron Transport Complex I - deficiency | Humans | NADH Dehydrogenase - genetics | Th2 Cells - immunology | Interleukin-2 - antagonists & inhibitors | Receptors, Antigen, T-Cell - antagonists & inhibitors | Th2 Cells - drug effects | Receptors, Antigen, T-Cell - biosynthesis | Lymphocyte Activation - immunology | DNA, Mitochondrial - genetics | Time Factors | Electron Transport Complex I - genetics | T-Lymphocytes - drug effects | Dermatitis, Atopic - immunology | Interleukin-4 - genetics | Immunosuppressive Agents - pharmacology | Electron Transport Complex I - antagonists & inhibitors | Interleukin-4 - antagonists & inhibitors | Gene Expression Regulation - immunology | Jurkat Cells | RNA, Small Interfering - pharmacology | Cells, Cultured | Ciprofloxacin - pharmacology | Immunophenotyping | Mitochondria - metabolism | Mitochondria - drug effects | Gene Expression Regulation - drug effects | Interleukin-2 - genetics | Interleukin-4 - secretion | Reactive Oxygen Species - antagonists & inhibitors | Lymphocyte Activation - drug effects | T-Lymphocytes - immunology | Receptors, Antigen, T-Cell - genetics | Interleukin-2 - secretion | Th2 Cells - enzymology
Journal Article
Neuroscience Letters, ISSN 0304-3940, 2010, Volume 486, Issue 3, pp. 235 - 239
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