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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
The EMBO Journal, ISSN 0261-4189, 02/2014, Volume 33, Issue 4, pp. 282 - 295
Journal Article
Circulation, ISSN 0009-7322, 05/2010, Volume 121, Issue 18, pp. 2012 - 2022
Background-Whether alterations in mitochondrial morphology affect the susceptibility of the heart to ischemia/reperfusion injury is unknown. We hypothesized... 
Myocardial infarction | Cardiomyocytes | Hypoxia | Reperfusion | Ischemia | hypoxia | PERMEABILITY TRANSITION PORE | APOPTOSIS | CARDIAC & CARDIOVASCULAR SYSTEMS | FUSION | myocardial infarction | REPERFUSION INJURY | DEATH | ischemia | cardiomyocytes | HL-1 CELLS | FLUCTUATIONS | MITOFUSIN-2 | PERIPHERAL VASCULAR DISEASE | DYSFUNCTION | HEMATOLOGY | reperfusion | Age Factors | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Male | Green Fluorescent Proteins - genetics | GTP Phosphohydrolases - antagonists & inhibitors | Mitochondria - ultrastructure | Mitochondrial Membranes - drug effects | Myocardial Reperfusion Injury - pathology | Transfection | Myocardial Reperfusion Injury - drug therapy | Quinazolinones - pharmacology | Cell Line | Myocytes, Cardiac - cytology | Mitochondrial Membranes - physiology | Mice, Inbred C57BL | Dynamins | Cardiotonic Agents - pharmacology | Microtubule-Associated Proteins - antagonists & inhibitors | Mitochondria - drug effects | Microscopy, Electron | Myocardial Reperfusion Injury - physiopathology | Microscopy, Confocal | Animals | GTP Phosphohydrolases - metabolism | Myocytes, Cardiac - drug effects | Cell Death - physiology | GTP Phosphohydrolases - genetics | Myocytes, Cardiac - physiology | Mitochondrial Membranes - ultrastructure | Mice | Membrane Fusion - physiology | Mitochondria - physiology
Journal Article
Science, ISSN 0036-8075, 12/2016, Volume 354, Issue 6318, pp. 1441 - 1444
Journal Article
The EMBO Journal, ISSN 0261-4189, 05/2013, Volume 32, Issue 9, pp. 1280 - 1292
Dynamin 1‐like protein (DNM1L) mediates fission of mitochondria and peroxisomes, and dysfunction of DNM1L has been implicated in several neurological... 
protein structure | dynamin superfamily GTPases | dynamin 1‐like protein | membrane remodelling | mitochondrial fission | dynamin 1-like protein | STALK REGION | FUSION | CRYSTAL-STRUCTURE | BIOCHEMISTRY & MOLECULAR BIOLOGY | PEROXISOMAL FISSION | DIVISION | DRP1 | CELL BIOLOGY | S-NITROSYLATION | CONFORMATIONAL-CHANGES | NUCLEOTIDE-FREE | GTPASE | Microtubule-Associated Proteins - chemistry | Mitochondrial Size - drug effects | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Humans | Cercopithecus aethiops | Crystallography, X-Ray | Mitochondrial Proteins - genetics | GTP Phosphohydrolases - antagonists & inhibitors | Mitochondrial Size - genetics | GTP Phosphohydrolases - chemistry | Mitochondria - genetics | Mitochondrial Proteins - metabolism | Protein Multimerization - physiology | Protein Structure, Quaternary - physiology | Protein Structure, Secondary | Mitochondrial Proteins - antagonists & inhibitors | RNA, Small Interfering - pharmacology | Models, Molecular | Mitochondria - metabolism | Microtubule-Associated Proteins - antagonists & inhibitors | Mitochondria - drug effects | Protein Folding | Mutation, Missense - physiology | Animals | GTP Phosphohydrolases - metabolism | GTP Phosphohydrolases - genetics | Models, Biological | Mitochondrial Proteins - chemistry | Mitochondria - physiology | COS Cells | Proteins | Mitochondria | Mutation | Neurological disorders | Crystal structure
Journal Article
Journal Article
Journal Article
Journal Article
Cancer Cell, ISSN 1535-6108, 02/2014, Volume 25, Issue 2, pp. 243 - 256
Mutations in are prevalent in human cancers and universally predictive of resistance to anticancer therapeutics. Although it is widely accepted that... 
ACTIVATION | INHIBITION | ONCOGENIC RAS | TUMOR PROGRESSION | CHK1 | ONCOLOGY | INITIATION | COMBINATION | SUPPRESSION | ATR | KINASES | CELL BIOLOGY | Neoplasms - metabolism | Protein Kinases - metabolism | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) - genetics | Humans | ras Proteins - metabolism | Drug Resistance, Neoplasm | Phosphatidylinositol 3-Kinases - metabolism | GTP Phosphohydrolases - antagonists & inhibitors | Ribosomal Protein S6 Kinases, 90-kDa - metabolism | Flow Cytometry | Neoplasms - genetics | DNA Damage - genetics | Female | Antineoplastic Agents - pharmacology | Membrane Proteins - metabolism | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | DNA Damage - drug effects | Proto-Oncogene Proteins - metabolism | Cell Survival - drug effects | Membrane Proteins - genetics | Proto-Oncogene Proteins - genetics | Mutation - genetics | Animals | GTP Phosphohydrolases - metabolism | Membrane Proteins - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - metabolism | GTP Phosphohydrolases - genetics | Mice, Nude | Proto-Oncogene Proteins p21(ras) - antagonists & inhibitors | Checkpoint Kinase 1 | Mice | Cell Transformation, Neoplastic - pathology | Neoplasms - pathology | Mitogen-Activated Protein Kinase 1 - metabolism | Chemotherapy | DNA damage | DNA | Genetic research | DNA repair | Cancer | Tumors
Journal Article
American Journal of Physiology - Lung Cellular and Molecular Physiology, ISSN 1040-0605, 11/2013, Volume 305, Issue 10, pp. L737 - L746
Mitochondria are dynamic organelles that continuously change their shape through fission and fusion. Disruption of mitochondrial dynamics is involved in... 
Mitochondria dynamics | Chronic obstructive pulmonary disease | GLOBAL BURDEN | OXIDATIVE STRESS | PHYSIOLOGY | FUSION | LIPID-PEROXIDATION | CREATINE-KINASE B | mitochondria dynamics | OBSTRUCTIVE PULMONARY-DISEASE | RESPIRATORY SYSTEM | DYNAMICS | FISSION | DYSFUNCTION | chronic obstructive pulmonary disease | COPD | RNA, Small Interfering - genetics | Epithelial Cells - metabolism | Reactive Oxygen Species - metabolism | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Epithelial Cells - drug effects | Humans | Cellular Senescence - drug effects | Mitochondrial Proteins - genetics | GTP Phosphohydrolases - antagonists & inhibitors | Immunoenzyme Techniques | Bronchi - drug effects | Mitochondrial Proteins - metabolism | Bronchi - metabolism | Membrane Proteins - metabolism | Bronchi - pathology | Membrane Proteins - genetics | Mitochondrial Proteins - antagonists & inhibitors | Cells, Cultured | Epithelial Cells - pathology | Mitochondria - metabolism | Microtubule-Associated Proteins - antagonists & inhibitors | Mitochondria - drug effects | Mitochondria - pathology | Microscopy, Electron | Blotting, Western | GTP Phosphohydrolases - metabolism | Membrane Proteins - antagonists & inhibitors | GTP Phosphohydrolases - genetics | Tobacco - adverse effects | Physiological aspects | Aging | Epithelial cells | Health aspects | Smoking
Journal Article