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Volumn 27, Issue 2, 2001, Pages 181-186
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Mouse models for Friedreich ataxia exhibit cardiomyopathy, sensory nerve defect and Fe-S enzyme deficiency followed by intramitochondrial iron deposits
a a a a b b a a c a |
Author keywords
[No Author keywords available]
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Indexed keywords
FRATAXIN;
IRON SULFUR PROTEIN;
ANIMAL EXPERIMENT;
ANIMAL MODEL;
ANIMAL TISSUE;
ARTICLE;
AUTOSOMAL RECESSIVE DISORDER;
CARDIOMYOPATHY;
CONTROLLED STUDY;
DISEASE SIMULATION;
ENZYME DEFICIENCY;
FRIEDREICH ATAXIA;
GENETIC ANALYSIS;
HISTOPATHOLOGY;
IRON OVERLOAD;
MITOCHONDRION;
MOUSE;
NERVE DEGENERATION;
NONHUMAN;
PRIORITY JOURNAL;
ANIMALS;
CARDIOMYOPATHIES;
FRIEDREICH ATAXIA;
GENE TARGETING;
HEREDITARY SENSORY AND AUTONOMIC NEUROPATHIES;
IRON-BINDING PROTEINS;
IRON-SULFUR PROTEINS;
MICE;
MICE, MUTANT STRAINS;
MITOCHONDRIA;
MUTAGENESIS;
PHOSPHOTRANSFERASES (ALCOHOL GROUP ACCEPTOR);
ANIMALIA;
ATAXIA;
MAMMALIA;
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EID: 0035138072
PISSN: 10614036
EISSN: None
Source Type: Journal
DOI: 10.1038/84818 Document Type: Article |
Times cited : (635)
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References (26)
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