Altered axonal architecture by removal of the heavily phosphorylated neurofilament tail domains strongly slows superoxide dismutase 1 mutant-mediated ALS

Proceedings of the National Academy of Sciences of the United States of America

Volumn 102, Issue 29, 2005, Pages 10351-10356

  Lobsiger, Christian S ^a   Garcia, Michael L ^a   Ward, Christopher M ^a,b   Cleveland, Don W ^a  

^a UNIVERSITY OF CALIFORNIA SAN DIEGO   (United States)

^b Cronkhite Graduate Center   (United States)

Author keywords

Axonal cytoskeleton; Axonal transport; Cyclin dependent kinase 5

Indexed keywords

COPPER ZINC SUPEROXIDE DISMUTASE; CYCLIN DEPENDENT KINASE 5; MUTANT PROTEIN; PROTEIN SUBUNIT;

AMYOTROPHIC LATERAL SCLEROSIS; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL SURVIVAL; CONTROLLED STUDY; CYTOSKELETON; GENE TARGETING; MOTONEURON; MOUSE; NERVE CELL LESION; NERVE FIBER; NERVE FIBER TRANSPORT; NEUROFILAMENT; NEUROTOXICITY; NONHUMAN; PHOSPHORYLATION; PRIORITY JOURNAL; PROTEIN DOMAIN;

AMYOTROPHIC LATERAL SCLEROSIS; ANIMALS; AXONS; CYCLIN-DEPENDENT KINASES; ELECTROPHORESIS, POLYACRYLAMIDE GEL; GENE TARGETING; IMMUNOBLOTTING; MICE; MICE, MUTANT STRAINS; MODELS, BIOLOGICAL; NEUROFILAMENT PROTEINS; PHOSPHORYLATION; PROTEIN STRUCTURE, TERTIARY; SUPEROXIDE DISMUTASE;

EID: 22544450456     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.0503862102     Document Type: Article

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