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Human Pathology, ISSN 0046-8177, 2015, Volume 49, pp. 27 - 32
Summary Complex I deficiency causes Leigh syndrome, fatal infant lactic acidosis, and neonatal cardiomyopathy. Mutations in more than 100 nuclear DNA and... 
Pathology | Metabolic disease | Lethal neonatal lactic acidosis | Whole-exome sequencing | Mitochondriopathy | Complex I deficiency | ACAD9 defect | Mitochondrial hyperplasia | Multiorgan failure | DIAGNOSIS | CARDIOMYOPATHY | PATHOLOGY | GENE | DNA | EXPRESSION | Immunohistochemistry | Fibroblasts - enzymology | Diaphragm - pathology | Mitochondria, Heart - pathology | Electron Transport Complex I - deficiency | Humans | Hyperplasia | Male | Cardiomyopathy, Hypertrophic - enzymology | Acyl-CoA Dehydrogenases - genetics | Leigh Disease - pathology | Muscle Weakness - genetics | Amino Acid Metabolism, Inborn Errors - genetics | Autopsy | DNA Mutational Analysis | Electron Transport Complex I - genetics | Fatal Outcome | Muscle Weakness - pathology | Acyl-CoA Dehydrogenases - deficiency | Amino Acid Metabolism, Inborn Errors - pathology | Kidney Tubules - pathology | Infant, Newborn | Multiple Organ Failure - pathology | Acyl-CoA Dehydrogenase - genetics | Cardiomyopathy, Hypertrophic - genetics | Genetic Predisposition to Disease | Mitochondria, Liver - pathology | Mitochondria, Heart - enzymology | Fibroblasts - pathology | Leigh Disease - genetics | Acidosis, Lactic - pathology | Cardiomyopathy, Hypertrophic - diagnosis | Mitochondrial Diseases - enzymology | Phenotype | Acyl-CoA Dehydrogenase - deficiency | Kidney Tubules - enzymology | Acidosis - diagnosis | Multiple Organ Failure - enzymology | Acidosis - genetics | Amino Acid Metabolism, Inborn Errors - enzymology | Mitochondrial Diseases - pathology | Muscle Weakness - diagnosis | Acidosis, Lactic - genetics | Cause of Death | Acidosis, Lactic - enzymology | Amino Acid Metabolism, Inborn Errors - diagnosis | DNA, Mitochondrial - genetics | Muscle Weakness - enzymology | Transfection | Mitochondrial Diseases - genetics | Mitochondria, Muscle - enzymology | Mitochondria, Muscle - pathology | Leigh Disease - enzymology | Cells, Cultured | Multiple Organ Failure - genetics | Codon, Nonsense | Mitochondria, Liver - enzymology | Multiple Organ Failure - diagnosis | Diaphragm - enzymology | Acidosis - pathology | Leigh Disease - diagnosis | Acidosis - enzymology | Mitochondrial Diseases - diagnosis | Acidosis, Lactic - diagnosis | Cardiomyopathy, Hypertrophic - pathology | Infants (Newborn) | Muscles | Genetic aspects | Mitochondrial DNA | Liver | Heart | Urine | Cytochrome | Antigens | Enzymes | Cytomegalovirus | Cardiomyopathy | Defects | Musculoskeletal system | Databases | Rodents | Fibroblasts | Oxidation | Mutation | Metabolic disorders | Deoxyribonucleic acid--DNA
Journal Article
Nature (London), ISSN 1476-4687, 2014, Volume 515, Issue 7527, pp. 431 - 435
Journal Article
The Journal of cell biology, ISSN 1540-8140, 2009, Volume 186, Issue 6, pp. 805 - 816
The dynamin-related guanosine triphosphatase Drp1 mediates the division of mitochondria and peroxisomes. To understand the in vivo function of Drp1, complete... 
Cerebellum | Mitochondria | Peroxisomes | Neurons | Antibodies | Cytochromes | Reports | Mice | Giant cells | Embryos | Apoptosis | OUTER-MEMBRANE | APOPTOSIS | DOMINANT OPTIC ATROPHY | FUSION | MITOCHONDRIAL FISSION MACHINERY | SYNAPSE FORMATION | CYTOCHROME-C RELEASE | PROTEIN DLP1 | DIVISION | CELL-DEATH | CELL BIOLOGY | Mitochondria - enzymology | Trophoblasts - ultrastructure | Fibroblasts - enzymology | Giant Cells - enzymology | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Trophoblasts - enzymology | Cerebellum - enzymology | Fibroblasts - ultrastructure | Mitochondria - ultrastructure | Purkinje Cells - enzymology | Cerebellum - embryology | Myocytes, Cardiac - enzymology | Adenosine Triphosphate - metabolism | Ultrasonography | Microtubule-Associated Proteins - deficiency | Purkinje Cells - diagnostic imaging | Mice, Inbred C57BL | Cells, Cultured | Dynamins | Gestational Age | Mice, Knockout | Organogenesis | Animals | GTP Phosphohydrolases - metabolism | GTP Phosphohydrolases - genetics | GTP Phosphohydrolases - deficiency | Peroxisomes - enzymology | Cerebellum - ultrastructure | Mitochondrial Size | Myocytes, Cardiac - ultrastructure | Organelle Shape | Peroxisomes - ultrastructure | Giant Cells - ultrastructure | Physiological aspects | Brain | Embryonic development | Research | Guanosine triphosphatase
Journal Article
Trends in Neurosciences, ISSN 0166-2236, 2012, Volume 35, Issue 11, pp. 700 - 709
Caspase-3 has been identified as a key mediator of neuronal programmed cell death. This protease plays a central role in the developing nervous system and its... 
Neurology | synaptic plasticity | synaptic loss | Alzheimer's disease | long-term depression | neuronal differentiation | long-term potentiation | Neuronal differentiation | Synaptic loss | Long-term depression | Long-term potentiation | Synaptic plasticity | ALZHEIMERS-DISEASE | MILD COGNITIVE IMPAIRMENT | NEUROSCIENCES | NEURODEGENERATIVE DISEASES | PROGRAMMED CELL-DEATH | MITOCHONDRIAL-MEMBRANE PERMEABILIZATION | PRECURSOR PROTEIN | HUNTINGTONS-DISEASE | PARKINSONS-DISEASE | Nerve Net - embryology | Mitochondria - enzymology | Caspase Inhibitors - pharmacology | Humans | Huntington Disease - pathology | Neurons - cytology | Nerve Net - enzymology | Molecular Targeted Therapy | Alzheimer Disease - pathology | Caspase 3 - physiology | Nervous System - growth & development | Nervous System - embryology | Huntington Disease - enzymology | Disease Models, Animal | Nerve Net - growth & development | Long-Term Synaptic Depression - physiology | Nerve Tissue Proteins - physiology | Nervous System - enzymology | Parkinson Disease - pathology | Embryonic Development - physiology | Neural Tube - physiology | Alzheimer Disease - enzymology | Receptors, N-Methyl-D-Aspartate - physiology | Mice, Knockout | Animals | Caspase Inhibitors - therapeutic use | Neurons - enzymology | Parkinson Disease - enzymology | Apoptosis Regulatory Proteins - physiology | Mice | Apoptosis - physiology | Enzyme Activation | Nervous system diseases | Neurosciences | Neural networks | Proteases | Neurons | Depression, Mental | Apoptosis | Neurodegenerative diseases | Proteinase | Central nervous system | Caspase-3 | Neurological diseases | Axons | Mitochondria | Neural tube | Plasticity (synaptic) | Reviews | Differentiation
Journal Article
The Journal of cell biology, ISSN 1540-8140, 2017, Volume 216, Issue 11, pp. 3655 - 3675
Axon degeneration is an early event and pathological in neurodegenerative conditions and nerve injuries. To discover agents that suppress neuronal death and... 
NEURONAL APOPTOSIS | AXON DEGENERATION | WALLERIAN DEGENERATION | SYMPATHETIC NEURONS | INHIBITOR FORETINIB | CYTOCHROME-C RELEASE | RECEPTOR TYROSINE-KINASE | NERVE GROWTH-FACTOR | CELL-DEATH | STATISTICAL-MODEL | CELL BIOLOGY
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