Caspase-1 and -3 are sequentially activated in motor neuron death in Cu,Zn superoxide dismutase-mediated familial amyotrophic lateral sclerosis.
Publication/Presentation Date
12-5-2000
Abstract
Familial amyotrophic lateral sclerosis-linked mutations in copper-zinc superoxide dismutase cause motor neuron death through one or more acquired toxic properties. An early event in the mechanism of toxicity from such mutants is now demonstrated to be activation of caspase-1. Neuronal death, however, follows only after months of chronic caspase-1 activation concomitantly with activation of the executioner caspase-3 as the final step in the toxic cascade. Thus, a common toxicity of mutant SOD1 is a sequential activation of at least two caspases, caspase-1 that acts slowly as a chronic initiator and caspase-3 acting as the final effector of cell death.
Volume
97
Issue
25
First Page
13901
Last Page
13906
ISSN
0027-8424
Published In/Presented At
Pasinelli, P., Houseweart, M. K., Brown, R. H., Jr, & Cleveland, D. W. (2000). Caspase-1 and -3 are sequentially activated in motor neuron death in Cu,Zn superoxide dismutase-mediated familial amyotrophic lateral sclerosis. Proceedings of the National Academy of Sciences of the United States of America, 97(25), 13901–13906. https://doi.org/10.1073/pnas.240305897
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
11095709
Department(s)
Administration and Leadership
Document Type
Article