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Neuron, ISSN 0896-6273, 04/2013, Volume 78, Issue 1, pp. 57 - 64
Valosin-containing protein (VCP) is a highly expressed member of the type II AAA+ ATPase family. mutations are the cause of inclusion body myopathy, Paget’s... 
LIPID-PEROXIDATION | SPINAL-CORD PATHOLOGY | MOUSE MODEL | ALS | AMYOTROPHIC-LATERAL-SCLEROSIS | DYSFUNCTION | BONE | NEUROSCIENCES | PAGET-DISEASE | TRANSGENIC MICE | REVEALS | RNA, Small Interfering - genetics | Humans | Middle Aged | Male | Frontotemporal Dementia - metabolism | Neurons - ultrastructure | Muscular Dystrophies, Limb-Girdle - genetics | Adenosine Triphosphate - metabolism | Membrane Potential, Mitochondrial - genetics | Muscular Dystrophies, Limb-Girdle - pathology | NAD - metabolism | Fibroblasts - metabolism | Animals, Newborn | Frontotemporal Dementia - genetics | Magnesium - metabolism | Mitochondria - pathology | Fibroblasts - pathology | Mutation - genetics | Myositis, Inclusion Body - genetics | Osteitis Deformans - pathology | Muscular Dystrophies, Limb-Girdle - metabolism | Analysis of Variance | Luminescent Proteins - genetics | Adenosine Triphosphatases - genetics | Mice | Lipid Peroxidation - genetics | RNA, Small Interfering - metabolism | Valosin Containing Protein | Osteitis Deformans - metabolism | Family Health | Cerebral Cortex - cytology | Case-Control Studies | Osteitis Deformans - genetics | Transfection | Mitochondria - genetics | Cell Cycle Proteins - genetics | Myositis, Inclusion Body - pathology | Adult | Female | Neuroblastoma - pathology | Frontotemporal Dementia - pathology | Adenosine Triphosphatases - deficiency | Mice, Inbred C57BL | Cells, Cultured | Cell Cycle Proteins - deficiency | Mitochondria - metabolism | Animals | Oxygen Consumption - genetics | Myositis, Inclusion Body - metabolism | Aged | Nervous system diseases | Neurosciences | Genes | Amyotrophic lateral sclerosis | Genetic aspects | Adenosine triphosphatase | Dementia | Proteins | Medical research | Phosphorylation | Biomedical research | Disease | Rodents | Respiration | Experiments | Patients | Report
Journal Article
Nature, ISSN 0028-0836, 07/2016, Volume 535, Issue 7613, pp. 561 - 565
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 08/2013, Volume 8, Issue 8, p. e70718
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 1/2011, Volume 108, Issue 1, pp. 314 - 318
Journal Article
PLoS Genetics, ISSN 1553-7390, 07/2017, Volume 13, Issue 7, p. e1006921
Several oxidative phosphorylation (OXPHOS) diseases are caused by defects in the post-transcriptional modification of mitochondrial tRNAs (mt-tRNAs). Mutations... 
LIFE-SPAN | GTP-BINDING PROTEIN | UNFOLDED PROTEIN RESPONSE | HYPERTROPHIC CARDIOMYOPATHY | STRESS RESPONSES | MEMBRANE-POTENTIALS | GENETICS & HEREDITY | NORTHERN BLOT METHOD | C-ELEGANS | LACTIC-ACIDOSIS | MODIFYING ENZYMES | Mitochondrial Diseases - genetics | Cell Nucleolus - genetics | Caenorhabditis elegans - genetics | Gene Expression - genetics | Electron Transport - genetics | Humans | Mitochondrial Diseases - metabolism | Oxidative Phosphorylation | Mitochondria - metabolism | Mitochondrial Proteins - genetics | Signal Transduction - genetics | GTP-Binding Proteins - genetics | Carrier Proteins - genetics | Animals | tRNA Methyltransferases - genetics | Mitochondria - genetics | RNA, Transfer - genetics | Mutation | Caenorhabditis elegans Proteins - genetics | Disease Models, Animal | Physiological aspects | Caenorhabditis elegans | Genetic aspects | Gene mutations | Observations | Transfer RNA | Pyrimidines | Liver diseases | Analysis | Electron transport | Tricarboxylic acid cycle | Post-transcription | Phosphorylation | Animal models | Transcription | Genes | Liver | Mitochondrial DNA | Defects | Proteins | Electron transport chain | Mitochondria | Bioenergetics | Metabolites | Fertility | Rewiring | Cell cycle | Heart diseases | Heart failure | tRNA Ala | Deactivation | tRNA | Therapeutic applications | Metabolism | Gene expression | Retrograde transport | Sterility | Life span | Acids | Oxidative phosphorylation | Nematodes | Uridine | Respiration | Basic Medicine | Medical Genetics | Medicinsk genetik | Medical and Health Sciences | Medicin och hälsovetenskap | Medicinska och farmaceutiska grundvetenskaper
Journal Article
PLoS Genetics, ISSN 1553-7390, 04/2018, Volume 14, Issue 4, p. e1007335
Gene expression variation is extensive in nature, and is hypothesized to play a major role in shaping phenotypic diversity. However, connecting differences in... 
HEAT-SHOCK PROTEINS | ETHANOL STRESS | NATURAL VARIATION | QUANTITATIVE TRAIT | TRANSCRIPTIONAL ACTIVATOR | GENETICS & HEREDITY | SACCHAROMYCES-CEREVISIAE STRAINS | HYDROGEN-PEROXIDE | RANDOMIZED CONTROLLED-TRIAL | GENOME-WIDE IDENTIFICATION | TRANSIENT ISCHEMIC ATTACKS | Oxidants - pharmacology | Catalase - genetics | Saccharomyces cerevisiae - genetics | Hydrogen Peroxide - pharmacology | Oxidants - metabolism | Chromosome Mapping | Drug Resistance, Fungal - genetics | Saccharomyces cerevisiae Proteins - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Hydrogen Peroxide - metabolism | Catalase - metabolism | Genetic Variation | Gene Expression Regulation, Fungal - drug effects | Ethanol - pharmacology | Phenotype | Cross Protection - genetics | Chromosomes, Fungal - genetics | Peroxidase - genetics | Gene Expression Regulation, Fungal - genetics | Peroxidase - metabolism | Quantitative Trait Loci - genetics | Microbiological research | Yeast fungi | Genetic variation | Genetic research | Genetic aspects | Research | Gene expression | Oxidative stress | Reactive oxygen species | Yeast | Hydrogen peroxide | Ethanol | Genomics | Phenotypic variations | Genomes | Quantitative trait loci | Proteins | Genotype & phenotype | Hypotheses | Catalase | Aerobic respiration | Heme | Genetics | Molecular biology | Gene mapping | Evolution & development | Strains (organisms) | Deoxyribonucleic acid--DNA | Deoxyribonucleic acid | DNA
Journal Article