Functional role of caspase-1 and caspase-3 in an ALS transgenic mouse model

Science

Volumn 288, Issue 5464, 2000, Pages 335-339

  Li, Mingwei ^a   Ona, Victor O ^a   Guégan, Christelle ^b   Chen, Minghua ^a   Jackson Lewis, Vernice ^b   Andrews, L John ^a   Olszewski, Adam J ^a   Stieg, Philip E ^a   Lee, Jean Pyo ^c   Przedborski, Serge ^b   Friedlander, Robert M ^a  

^a HARVARD MEDICAL SCHOOL   (United States)

^b Columbia University ^*  (United States)

^c UNIVERSITY OF CHICAGO   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CASPASE 3; CASPASE INHIBITOR; COPPER ZINC SUPEROXIDE DISMUTASE; INTERLEUKIN 1BETA CONVERTING ENZYME; MESSENGER RNA; MUTANT PROTEIN;

AMINO ACID SUBSTITUTION; AMYOTROPHIC LATERAL SCLEROSIS; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DEGENERATIVE DISEASE; DRUG EFFECT; ENZYME INHIBITION; FATALITY; GENE EXPRESSION REGULATION; GENE MUTATION; NEUROPROTECTION; NONHUMAN; PRIORITY JOURNAL; TRANSGENIC MOUSE;

AMINO ACID CHLOROMETHYL KETONES; AMINO ACID SUBSTITUTION; AMYOTROPHIC LATERAL SCLEROSIS; ANIMALS; APOPTOSIS; CASPASE 1; CASPASE 3; CASPASES; CYSTEINE PROTEINASE INHIBITORS; DISEASE MODELS, ANIMAL; DISEASE PROGRESSION; ENZYME ACTIVATION; GENE EXPRESSION REGULATION, ENZYMOLOGIC; HUMANS; INJECTIONS, INTRAVENTRICULAR; INTERLEUKIN-1; MALE; MICE; MICE, TRANSGENIC; MOTOR NEURONS; NERVE DEGENERATION; NEUROPROTECTIVE AGENTS; PSYCHOMOTOR PERFORMANCE; SPINAL CORD; SUPEROXIDE DISMUTASE;

ANIMALIA; MUS MUSCULUS; RODENTIA;

EID: 0034647003     PISSN: 00368075     EISSN: None     Source Type: Journal    
DOI: 10.1126/science.288.5464.335     Document Type: Article

References (37)

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37. We thank A. Srinivasan for providing the CM1 antibody and J. Yuan for providing the caspase-1 antibody; M. Schoenebeck for expert preparation of the phrenic nerve samples; J. Yuan for insightful comments on the manuscript; and E. Friedlander for editorial assistance. Supported by the Muscular Dystrophy Association; the ALS Association; Project-ALS; the National Institute of Neurological Disorders and Stroke (grants R01 NS38586, R29 NS37345, and P50 NS38370); the U.S. Department of Defense (grant DAMD 17-99-1-9471); the Lowenstein Foundation; the Smart Foundation; and the Parkinson's Disease Foundation. C.G. is the recipient of a scholarship from the French ISERM. S.P. is a recipient of the Cotzias Award from the American Parkinson Disease Association.