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Journal Article
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 | Data bases | Defects | Musculoskeletal system | Rodents | Fibroblasts | Oxidation | Mutation | Metabolic disorders | Deoxyribonucleic acid--DNA | Index Medicus
Journal Article
Journal Article
Journal of Histochemistry and Cytochemistry, ISSN 0022-1554, 02/2006, Volume 54, Issue 2, pp. 191 - 199
Journal Article
Journal Article
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 508, Issue 7495, pp. 258 - 262
In obesity and type 2 diabetes, Glut4 glucose transporter expression is decreased selectively in adipocytes(1). Adipose-specific knockout or overexpression of... 
OXIDATIVE STRESS | METABOLISM | INSULIN-RESISTANCE | MULTIDISCIPLINARY SCIENCES | LIVER | MOUSE | MICE | CDNA CLONING | EXPRESSION | SIRT1 | ADIPOSE-TISSUE | Sirtuin 1 - metabolism | Acetyltransferases - metabolism | Adipocytes - secretion | Ornithine Decarboxylase - metabolism | Liver - enzymology | Glucose Transporter Type 4 - metabolism | Adipose Tissue, White - metabolism | Male | Diabetes Mellitus, Type 2 - metabolism | Nicotinamide N-Methyltransferase - metabolism | Glucose Intolerance | Glucose Transporter Type 4 - deficiency | Obesity - genetics | Thinness - metabolism | Gene Knockdown Techniques | Adipose Tissue - metabolism | Nicotinamide N-Methyltransferase - deficiency | Obesity - etiology | NAD - metabolism | Spermine - analogs & derivatives | Nicotinamide N-Methyltransferase - genetics | Thinness - enzymology | Glucose Transporter Type 4 - genetics | Niacinamide - metabolism | Mice, Inbred C57BL | Diabetes Mellitus, Type 2 - enzymology | Insulin Resistance | Oxidoreductases Acting on CH-NH Group Donors - metabolism | Fatty Liver | Animals | Diet | Energy Metabolism | Adipocytes - metabolism | Obesity - prevention & control | Spermine - metabolism | Adipose Tissue, White - enzymology | Adipose Tissue - enzymology | Mice | Obesity - enzymology | S-Adenosylmethionine - metabolism | Adipose tissues | Type 2 diabetes | Obesity | Care and treatment | Analysis | Transferases | Physiological aspects | Genetic aspects | Research | Gene expression | Enzymes | Body fat | Adipocytes | Polyamines | Variance analysis | Proteins | Weight control | Metabolites | Rodents | Insulin resistance | Diabetes | Mass spectrometry | Food | Index Medicus
Journal Article
Biochemical Journal, ISSN 0264-6021, 08/2004, Volume 381, Issue 3, pp. 761 - 767
An important regulator involved in oxygen-dependent gene expression is the transcription factor HIF (hypoxia-inducible factor), which is composed of an... 
Post-translational modification | Hypoxia-inducible factor | Protein degradation | Oxygen sensing | Prolyl hydroxylation | Von-Hippel-Lindau protein | TRANSCRIPTIONAL ACTIVITY | PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | ALPHA | hypoxia-inducible factor | oxygen sensing | post-translational modification | von-Hippel-Lindau protein | FAMILY | OXYGEN | FACTOR-1-ALPHA | GENE-EXPRESSION | HIF-1-ALPHA | VHL | protein degradation | prolyl hydroxylation | Humans | Half-Life | Kidney Neoplasms - metabolism | Ubiquitin-Protein Ligases - physiology | Bone Neoplasms - pathology | Hypoxia-Inducible Factor 1, alpha Subunit | RNA, Messenger - biosynthesis | Liver Neoplasms - pathology | Liver Neoplasms - enzymology | Kidney Tubules, Proximal - cytology | DNA-Binding Proteins - physiology | Hypoxia - enzymology | Hydroxylation | Hypoxia-Inducible Factor 1 | Immediate-Early Proteins - biosynthesis | Carcinoma, Hepatocellular - enzymology | Tumor Suppressor Proteins - physiology | Epithelial Cells - enzymology | Liver Neoplasms - metabolism | Cell Line, Tumor | Von Hippel-Lindau Tumor Suppressor Protein | Enzyme Induction - physiology | Osteosarcoma - pathology | Carcinoma, Hepatocellular - metabolism | Epithelial Cells - metabolism | Gene Expression Regulation, Enzymologic - physiology | Oxygen - metabolism | Procollagen-Proline Dioxygenase - biosynthesis | Bone Neoplasms - metabolism | Procollagen-Proline Dioxygenase - metabolism | DNA-Binding Proteins - metabolism | Kidney Tubules, Proximal - enzymology | Gene Expression Regulation, Neoplastic - physiology | Osteosarcoma - metabolism | Cell Line | Transcription Factors - physiology | Bone Neoplasms - enzymology | Osteosarcoma - enzymology | Adenocarcinoma, Clear Cell - metabolism | Nuclear Proteins - metabolism | Hypoxia-Inducible Factor-Proline Dioxygenases | Dioxygenases | Transcription Factors - metabolism | Kidney Neoplasms - enzymology | Carcinoma, Hepatocellular - pathology | Kidney Tubules, Proximal - metabolism | Kidney Neoplasms - pathology | Adenocarcinoma, Clear Cell - pathology | Nuclear Proteins - physiology | Adenocarcinoma, Clear Cell - enzymology | DNA-Binding Proteins - biosynthesis | Index Medicus | ODD, oxygen-dependent degradation domain | aRP, acidic ribosomal protein | RNAi, RNA interference | pVHL, von-Hippel-Lindau protein | EGLN, egg-laying deficient nine-like protein | HIF, hypoxia-inducible factor | siRNA, small interfering RNA | IVTT, in vitro transcription | PHD, prolyl hydroxylase domain containing protein | translation | RT, reverse transcriptase | RPTEC, human renal proximal tubular epithelial cells
Journal Article
Journal Article
Proceedings of the National Academy of Sciences, ISSN 0027-8424, 11/2014, Volume 111, Issue 45, pp. E4878 - E4886
Inflammation is accompanied by the release of highly reactive oxygen and nitrogen species (RONS) that damage DNA, among other cellular molecules. Base excision... 
Aag/Mpg DNA glycosylase | DNA repair | Ischemia reperfusion | Liver | Base excision | GLYCOSYLASE | liver | MULTIDISCIPLINARY SCIENCES | DNA-DAMAGE | ischemia reperfusion | MECHANISMS | HMGB1 | CELL-DEATH | PROTECTS | PATHWAY | base excision | INFLAMMATION | POLY(ADP-RIBOSE) POLYMERASE-1 | STRESS | Inflammation - pathology | Liver - pathology | Liver - enzymology | Reactive Oxygen Species - metabolism | Kidney - pathology | Kidney - enzymology | Brain - enzymology | Brain Infarction - pathology | Hepatocytes - pathology | Acute Kidney Injury - genetics | HMGB1 Protein - genetics | HMGB1 Protein - metabolism | Cell Death | Reperfusion Injury - genetics | DNA Glycosylases - metabolism | Brain Infarction - enzymology | Reperfusion Injury - pathology | Acute Kidney Injury - pathology | Reactive Nitrogen Species - metabolism | Reperfusion Injury - enzymology | DNA Glycosylases - genetics | Acute Kidney Injury - enzymology | Mice, Knockout | Enzyme Induction - genetics | Poly(ADP-ribose) Polymerases - metabolism | Animals | Poly(ADP-ribose) Polymerases - genetics | DNA Repair | Brain - pathology | Inflammation - genetics | Mice | DNA Damage | Brain Infarction - genetics | Inflammation - enzymology | Hepatocytes - enzymology | Brain | Kidneys | DNA polymerase | Rodents | DNA damage | Index Medicus | Biological Sciences | PNAS Plus | Aag | Mpg DNA glycosylase
Journal Article