Targeting ATM ameliorates mutant Huntingtin toxicity in cell and animal models of Huntington’s disease
Copyright policy )Targeting ATM ameliorates mutant Huntingtin toxicity in cell and animal models of Huntington’s disease
Reducing ATM signaling is neuroprotective in cell and animal models of Huntington’s disease.
- CHDI Foundation United States
- Baylor College of Medicine United States
- National Institute of Health Pakistan
- University of Auckland New Zealand
- University of California, Los Angeles United States
Adult, Huntingtin Protein, Behavior, Animal, Morpholines, Induced Pluripotent Stem Cells, Gene Dosage, Brain, Ataxia Telangiectasia Mutated Proteins, Middle Aged, Cell Line, Histones, Disease Models, Animal, Mice, Neurologic Mutants, Drosophila melanogaster, Huntington Disease, Cytoprotection, Gene Knockdown Techniques, Animals, Humans, Aged
Adult, Huntingtin Protein, Behavior, Animal, Morpholines, Induced Pluripotent Stem Cells, Gene Dosage, Brain, Ataxia Telangiectasia Mutated Proteins, Middle Aged, Cell Line, Histones, Disease Models, Animal, Mice, Neurologic Mutants, Drosophila melanogaster, Huntington Disease, Cytoprotection, Gene Knockdown Techniques, Animals, Humans, Aged
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