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Free Radical Biology and Medicine, ISSN 0891-5849, 11/2017, Volume 112, pp. 336 - 349
Aberrant modulation of mitochondrial dynamic network, which shifts the balance of fusion and fission towards fission, is involved in brain damage of various... 
Mdivi-1 | Inflammation | Early brain injury | Blood-brain barrier disruption | Subarachnoid hemorrhage | Apoptosis | OXYGEN SPECIES PRODUCTION | OXIDATIVE STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | COMPLEX I INHIBITOR | HIPPOCAMPAL-NEURONS | RAT MODEL | MITOCHONDRIAL FISSION | CELL-DEATH | SIGNALING PATHWAY | MOUSE MODEL | ENDOCRINOLOGY & METABOLISM | NF-KAPPA-B | Interleukin-6 - antagonists & inhibitors | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Proto-Oncogene Proteins c-bcl-2 - agonists | Tumor Necrosis Factor-alpha - genetics | Male | NF-kappa B - metabolism | Interleukin-1beta - genetics | Subarachnoid Space - drug effects | Occludin - metabolism | Matrix Metalloproteinase 9 - metabolism | Interleukin-1beta - metabolism | Matrix Metalloproteinase 9 - genetics | Subarachnoid Hemorrhage - mortality | Zonula Occludens-1 Protein - metabolism | Interleukin-6 - metabolism | Subarachnoid Hemorrhage - drug therapy | Interleukin-1beta - antagonists & inhibitors | Zonula Occludens-1 Protein - genetics | NF-kappa B - antagonists & inhibitors | Endoplasmic Reticulum Stress - drug effects | Interleukin-6 - genetics | bcl-2-Associated X Protein - metabolism | Dynamins - genetics | Rats | Subarachnoid Hemorrhage - genetics | Rats, Sprague-Dawley | Blood-Brain Barrier - metabolism | Reactive Oxygen Species - antagonists & inhibitors | Survival Analysis | Subarachnoid Space - metabolism | Tumor Necrosis Factor-alpha - metabolism | Dynamins - metabolism | Mitochondrial Dynamics - genetics | Claudin-5 - metabolism | Occludin - genetics | Proto-Oncogene Proteins c-bcl-2 - metabolism | Mitochondria - genetics | Quinazolinones - pharmacology | bcl-2-Associated X Protein - genetics | Dynamins - antagonists & inhibitors | Claudin-5 - genetics | Mitochondria - metabolism | Mitochondria - drug effects | Subarachnoid Hemorrhage - pathology | bcl-2-Associated X Protein - antagonists & inhibitors | Blood-Brain Barrier - drug effects | Animals | Mitochondrial Dynamics - drug effects | NF-kappa B - genetics | Subarachnoid Space - pathology | Proto-Oncogene Proteins c-bcl-2 - genetics | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Stroke (Disease) | Proteins | Medical research | Brain | Neurons | Analysis | Medicine, Experimental | Brain damage | Injuries | Index Medicus
Journal Article
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 | Index Medicus
Journal Article
by Liu, T and Roh, S.E and Woo, J.A and Ryu, H and Kang, D.E
Cell death & disease, ISSN 2041-4889, 2013, Volume 4, Issue 1, pp. e476 - e476
Mitochondrial dysfunction and synaptic damage are critical early features of Alzheimer's disease (AD) associated with amyloid beta (Ab) and tau. We previously... 
BAX EXPRESSION | TRANSLOCATION | ACTIVATION | cofilin | PHOSPHORYLATION | mitochondria | apoptosis | BETA-PEPTIDE | AMYLOID PRECURSOR PROTEIN | p73 | CELL BIOLOGY | BCL-2 | amyloid | RanBPM | DYSFUNCTION | ACCUMULATION | PIVOTAL ROLE | Cyclin D1 - metabolism | Cytoskeletal Proteins - antagonists & inhibitors | Tumor Suppressor Proteins - antagonists & inhibitors | Cytoskeletal Proteins - genetics | Membrane Potential, Mitochondrial - drug effects | DNA-Binding Proteins - metabolism | Caspases - metabolism | RNA Interference | Adaptor Proteins, Signal Transducing - antagonists & inhibitors | Tumor Suppressor Proteins - genetics | Amyloid beta-Peptides - metabolism | Superoxides - metabolism | Cytoskeletal Proteins - metabolism | Nuclear Proteins - genetics | Quinazolinones - pharmacology | Peptide Fragments - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Cytochromes c - metabolism | Cells, Cultured | bcl-2-Associated X Protein - metabolism | Mice, Transgenic | Nuclear Proteins - metabolism | Mitochondria - metabolism | DNA-Binding Proteins - genetics | Hippocampus - cytology | Hippocampus - metabolism | Tumor Protein p73 | Animals | Nuclear Proteins - antagonists & inhibitors | Adaptor Proteins, Signal Transducing - genetics | X-Linked Inhibitor of Apoptosis Protein - metabolism | Protein Binding | Mice | Adaptor Proteins, Signal Transducing - metabolism | bcl-X Protein - metabolism | Apoptosis | RNA, Small Interfering - metabolism | Index Medicus | Original
Journal Article
Biochemical Journal, ISSN 0264-6021, 06/2017, Volume 474, Issue 11, pp. 1867 - 1877
Until recently, one of the major limitations of hydrogen/deuterium exchange mass spectrometry (HDX-MS) was the peptide-level resolution afforded by proteolytic... 
ACTIVATION | AMIDE HYDROGENS | PROTEIN | HDX-MS | MEMBRANE | BIOCHEMISTRY & MOLECULAR BIOLOGY | INTRAMOLECULAR MIGRATION | KINASE | IDENTIFICATION | CAPTURE DISSOCIATION | BINDING | Oligonucleotides - genetics | Oligonucleotides - chemistry | Class Ia Phosphatidylinositol 3-Kinase - metabolism | Electron Transport | Molecular Weight | Humans | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Enzyme Inhibitors - chemistry | Oligonucleotides - antagonists & inhibitors | Signal Processing, Computer-Assisted | Binding Sites | Peptide Fragments - genetics | Drug Evaluation, Preclinical - methods | Triazines - metabolism | Triazines - pharmacology | Indazoles - chemistry | Enzyme Inhibitors - metabolism | Purines - metabolism | Enzyme Inhibitors - pharmacology | Models, Molecular | Indazoles - metabolism | Recombinant Fusion Proteins - chemistry | Sulfonamides - pharmacology | Class Ia Phosphatidylinositol 3-Kinase - antagonists & inhibitors | Indazoles - pharmacology | Oligonucleotides - metabolism | Peptide Fragments - chemistry | Class I Phosphatidylinositol 3-Kinases | Purines - chemistry | Peptide Fragments - antagonists & inhibitors | Protein Conformation | Quinazolinones - chemistry | Quinazolinones - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Recombinant Fusion Proteins - metabolism | Quinolines - pharmacology | Antineoplastic Agents - metabolism | Tandem Mass Spectrometry | Class Ia Phosphatidylinositol 3-Kinase - chemistry | Deuterium Exchange Measurement | Triazines - chemistry | Antineoplastic Agents - pharmacology | Class Ia Phosphatidylinositol 3-Kinase - genetics | Quinazolinones - pharmacology | Peptide Fragments - metabolism | Reproducibility of Results | Sulfonamides - chemistry | Purines - pharmacology | Quinolines - chemistry | Phosphatidylinositol 3-Kinases - chemistry | Antineoplastic Agents - chemistry | Phosphatidylinositol 3-Kinases - genetics | Quinolines - metabolism | Sulfonamides - metabolism | Index Medicus | 1 | s | 4 | ETD | PI3K | 39 | MS | 8 | 10
Journal Article
BBA - Molecular Basis of Disease, ISSN 0925-4439, 02/2014, Volume 1842, Issue 2, pp. 220 - 231
Mitochondrial dysfunction is an early pathological feature of Alzheimer’s disease (AD). The underlying mechanisms and strategies to repair it remain unclear.... 
DLP1 | Mitochondrial fission and fusion | Alzheimer's disease | Cybrid cells | ERK | PATHWAYS | OXIDATIVE-PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | TOXICITY | MAMMALIAN-CELLS | BIOPHYSICS | AMYLOID-BETA | A-BETA | OXIDANT-STRESS | DYNAMICS | FISSION | PROTEINS | Neurons - pathology | Reactive Oxygen Species - metabolism | Microtubule-Associated Proteins - genetics | Mitochondrial Dynamics - genetics | Microtubule-Associated Proteins - metabolism | Humans | Middle Aged | Immunoblotting | Male | Mitochondrial Proteins - genetics | Extracellular Signal-Regulated MAP Kinases - metabolism | Alzheimer Disease - pathology | Probucol - pharmacology | Mitochondria - genetics | RNA Interference | Mitochondrial Proteins - metabolism | Aged, 80 and over | Female | Neurons - metabolism | Quinazolinones - pharmacology | Hybrid Cells - metabolism | Mitochondria - metabolism | Signal Transduction - genetics | Antioxidants - pharmacology | Mitochondria - drug effects | GTP Phosphohydrolases - metabolism | Mitochondrial Dynamics - drug effects | Hybrid Cells - pathology | Mitogen-Activated Protein Kinase 3 - metabolism | Signal Transduction - drug effects | GTP Phosphohydrolases - genetics | Models, Biological | Alzheimer Disease - metabolism | Aged | Mutation | Alzheimer Disease - genetics | Mitogen-Activated Protein Kinase 1 - metabolism | Genetic engineering | Mitochondrial DNA | Amyloid beta-protein | Index Medicus
Journal Article
Journal Article
Molecular Neurobiology, ISSN 0893-7648, 1/2016, Volume 53, Issue 1, pp. 240 - 253
This study aimed to examine whether the neuroprotective effects of Mdivi-1 are attributable to extracellular ATP and adenosine. Mdivi-1 was administered prior... 
Neurology | Neurosciences | Adenosine | Cerebral ischemia | Biomedicine | cAMP response element-binding protein | Neurobiology | CD39 | Mdivi-1 | Regional cerebral blood flow | Cell Biology | cerebralbloodflow | RAT STRIATUM | TISSUE-DAMAGE | Regional | OUTER-MEMBRANE PERMEABILIZATION | NEUROSCIENCES | NUCLEOSIDE TRANSPORTERS | cAMPresponseelement-bindingprotein | INHIBITION | IN-VIVO | CENTRAL-NERVOUS-SYSTEM | CEREBRAL-BLOOD-FLOW | RECEPTORS | ATP | Dynamins - metabolism | Recovery of Function - drug effects | Quinazolinones - administration & dosage | Male | Antigens, CD - metabolism | Extracellular Space - metabolism | Neuroprotective Agents - pharmacology | Adenosine Triphosphate - metabolism | Cyclic AMP - metabolism | Quinazolinones - pharmacology | Astrocytes - drug effects | Mice, Inbred C57BL | Apyrase - metabolism | Cells, Cultured | Brain Ischemia - physiopathology | Brain Ischemia - prevention & control | Blood-Brain Barrier - drug effects | Receptor, Adenosine A1 - metabolism | Blood-Brain Barrier - metabolism | Hydrolysis | Up-Regulation - drug effects | Blood-Brain Barrier - pathology | Animals | Signal Transduction - drug effects | Brain Ischemia - drug therapy | Brain Ischemia - pathology | Cyclic AMP Response Element-Binding Protein - metabolism | Adenosine - metabolism | Quinazolinones - therapeutic use | Astrocytes - metabolism | Stroke (Disease) | Brain | Analysis | High performance liquid chromatography | Injuries | Protein binding | Neurophysiology | Proteins | Phosphorylation | Stroke | Ischemia | Index Medicus
Journal Article
Cell Death and Disease, ISSN 2041-4889, 01/2015, Volume 6, Issue 1, pp. e1593 - e1593
Journal Article
The Journal of Clinical Endocrinology & Metabolism, ISSN 0021-972X, 05/2013, Volume 98, Issue 5, pp. 2153 - 2159
Context: Graves ophthalmopathy (GO) is an autoimmune disorder characterized by increased adipogenesis and hyaluronan (HA) production by orbital fibroblasts.... 
AUTOIMMUNITY | DISEASE | ENDOCRINOLOGY & METABOLISM | STIMULATING HORMONE-RECEPTOR | UPDATE | CAMP PRODUCTION | PREADIPOCYTE FIBROBLASTS | AGONIST | Eye - pathology | Thyrotropin - agonists | Receptors, Thyrotropin - agonists | Adipose Tissue, White - immunology | Humans | Adipose Tissue, White - metabolism | Cell Dedifferentiation | Eye - immunology | Graves Ophthalmopathy - metabolism | Osmolar Concentration | Protein Processing, Post-Translational - drug effects | Thyrotropin - pharmacology | Immunoglobulins, Thyroid-Stimulating - metabolism | Thyrotropin - antagonists & inhibitors | Eye - drug effects | Phosphorylation - drug effects | Graves Ophthalmopathy - drug therapy | Proto-Oncogene Proteins c-akt - metabolism | Cyclic AMP - metabolism | Quinazolinones - pharmacology | Fibroblasts - metabolism | Eye - metabolism | Adipose Tissue, White - pathology | Receptors, Thyrotropin - metabolism | Cells, Cultured | Receptors, Thyrotropin - antagonists & inhibitors | Fibroblasts - pathology | Graves Ophthalmopathy - immunology | Signal Transduction - drug effects | Drug Inverse Agonism | Fibroblasts - drug effects | Hyaluronic Acid - metabolism | Fibroblasts - immunology | Graves Ophthalmopathy - pathology | Pyridines - pharmacology | Antibodies, Monoclonal - metabolism | Adipose Tissue, White - drug effects | Index Medicus | Abridged Index Medicus | Endocrine Research
Journal Article
Leukemia, ISSN 0887-6924, 09/2018, Volume 32, Issue 9, pp. 1958 - 1969
The PI 3-kinases (PI3K) are essential mediators of chemokine receptor signaling necessary for migration of chronic lymphocytic leukemia (CLL) cells and their... 
G-BETA-GAMMA | P110-GAMMA ISOFORM | ONCOLOGY | PHOSPHATIDYLINOSITOL 3-KINASE | REGULATORY SUBUNITS | CHRONIC LYMPHOCYTIC-LEUKEMIA | SURVIVAL SIGNALS | ZAP-70 EXPRESSION | HEMATOLOGY | MARROW STROMAL CELLS | T-LYMPHOCYTES | DIFFERENTIAL ROLES | Leukemia, B-Cell - metabolism | Class I Phosphatidylinositol 3-Kinases - genetics | Class I Phosphatidylinositol 3-Kinases - metabolism | Class Ib Phosphatidylinositol 3-Kinase - genetics | Humans | Cell Survival - genetics | Lymphoma, B-Cell - genetics | Cell Movement - genetics | Gene Knockdown Techniques | CD40 Ligand - metabolism | Class Ib Phosphatidylinositol 3-Kinase - metabolism | ZAP-70 Protein-Tyrosine Kinase - metabolism | Antineoplastic Agents - pharmacology | B-Lymphocytes - pathology | Gene Expression Regulation, Neoplastic - drug effects | Mesenchymal Stem Cells - metabolism | B-Lymphocytes - metabolism | Quinazolinones - pharmacology | Cell Survival - drug effects | Cell Adhesion - genetics | Lymphoma, B-Cell - metabolism | Purines - pharmacology | Interleukin-4 - metabolism | Leukemia, B-Cell - pathology | Cell Adhesion - drug effects | Chemotaxis - genetics | Class I Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Cell Movement - drug effects | Leukemia, B-Cell - genetics | Lymphoma, B-Cell - pathology | Cytoskeleton - metabolism | Chemokines - metabolism | Class Ib Phosphatidylinositol 3-Kinase - antagonists & inhibitors | Mutation | Immunoglobulin Heavy Chains - genetics | CXCL12 protein | Leukocyte migration | Leukemia | Cytology | Adhesion tests | ZAP-70 protein | Kinases | CD40L protein | Cell morphology | Cell adhesion & migration | Interleukin 4 | Actin | Inhibition | Chronic lymphatic leukemia | Crosslinking | Lymphatic leukemia | Adhesion | 1-Phosphatidylinositol 3-kinase | Inhibitors | Lymphocytes B | Morphology | Stromal cells | Cell lines | Chemokines | Cell migration | Index Medicus
Journal Article
Journal of Nephrology, ISSN 1121-8428, 2013, Volume 26, Issue 6, pp. 1073 - 1082
Introduction: Mitochondrial dysfunction plays an important role in acute kidney injury (AKI). Mitochondrial fission regulated by dynamin-related protein 1... 
Mitochondria | Rhabdomyolysis | Dynaminrelated protein 1 | Acute kidney injury | Apoptosis | CELLS | ACTIVATION | ACID | RATS | MECHANISMS | H2O2 | FAILURE | Dynamin-related protein 1 | DISEASE | UROLOGY & NEPHROLOGY | FISSION | Dynamins - metabolism | Reactive Oxygen Species | Kidney - pathology | Myoglobin - metabolism | Epithelial Cells - drug effects | Caspase 3 - metabolism | Mitochondrial Diseases - metabolism | Rhabdomyolysis - complications | Male | Adenosine Triphosphate - biosynthesis | Mitochondrial Diseases - etiology | Mitochondrial Dynamics - physiology | Mitochondrial Proteins - metabolism | Membrane Proteins - metabolism | Kidney Tubules - pathology | Acute Kidney Injury - etiology | Kidney - physiopathology | Quinazolinones - pharmacology | Solvents | Mitochondrial Diseases - prevention & control | Kidney - drug effects | Kidney Tubules - drug effects | Cytochromes c - metabolism | bcl-2-Associated X Protein - metabolism | Glycerol | Kidney Tubules - ultrastructure | Rats | Mitochondria - metabolism | Rats, Sprague-Dawley | Acute Kidney Injury - prevention & control | Rhabdomyolysis - metabolism | Animals | Mitochondrial Dynamics - drug effects | Creatinine - blood | Rhabdomyolysis - chemically induced | Cytosol - metabolism | Apoptosis - physiology | Acute Kidney Injury - metabolism | Proliferating Cell Nuclear Antigen - metabolism
Journal Article
BMC Neuroscience, ISSN 1471-2202, 06/2016, Volume 17, Issue 1, pp. 33 - 33
Background: Kainic acid (KA)-induced excitotoxicity promotes cytoplasmic calcium accumulation, oxidative stress, and apoptotic signaling, leading to... 
Neuroinflammation | Mitochondrial fission | Neuronal cell death | Drp1 | TEMPORAL-LOBE EPILEPSY | STATUS EPILEPTICUS | OUTER-MEMBRANE PERMEABILIZATION | APOPTOSIS PROTEIN | NEUROSCIENCES | NEURODEGENERATIVE DISEASES | INDUCED SEIZURES | CYCLOPHILIN-D | NEURONAL DEATH | LINKED INHIBITOR | RAT HIPPOCAMPUS | Neurons - pathology | Dynamins - metabolism | Neuroglia - pathology | Seizures - drug therapy | Male | Neuroimmunomodulation - physiology | Seizures - metabolism | Hippocampus - drug effects | Kainic Acid | Mitochondrial Dynamics - physiology | Neuroglia - drug effects | Neuroprotective Agents - pharmacology | Seizures - pathology | Microfilament Proteins - metabolism | Neurons - metabolism | Cell Death - drug effects | Neurons - drug effects | Quinazolinones - pharmacology | Disease Models, Animal | Calcium-Binding Proteins - metabolism | Ubiquitin-Protein Ligases - metabolism | HSP72 Heat-Shock Proteins - metabolism | Hippocampus - pathology | Mitochondria - metabolism | Mitochondria - drug effects | Mitochondria - pathology | Random Allocation | Mitochondrial Degradation - physiology | Mice, Inbred ICR | Hippocampus - metabolism | Animals | Mitochondrial Dynamics - drug effects | Cell Death - physiology | Mitochondrial Degradation - drug effects | Cyclooxygenase 2 - metabolism | Survival Analysis | Neuroglia - metabolism | Neuroimmunomodulation - drug effects | Physiological aspects | Mitochondria | Research | Neurons | Kainic acid | Apoptosis | Index Medicus
Journal Article