In:
FEBS Letters, Wiley, Vol. 503, No. 2-3 ( 2001-08-17), p. 201-205
Abstract:
Approximately 10% of all familial cases of amyotrophic lateral sclerosis (fALS) are linked to mutations in the SOD1 gene, which encodes the copper/zinc superoxide dismutase (CuZnSOD). Recently, wild‐type CuZnSOD was shown to protect calcineurin, a calcium/calmodulin‐regulated phosphoprotein phosphatase, from inactivation by reactive oxygen species. We asked whether the protective effect of CuZnSOD on calcineurin is affected by mutations associated with fALS. For this, we monitored calcineurin activity in the presence of mutant and wild‐type SOD. We found that the degree of protection against inactivation of calcineurin by different SOD mutants correlates with the severity of the phenotype associated with the different mutations, suggesting a potential role for calcineurin–SOD1 interaction in the etiology of fALS.
Type of Medium:
Online Resource
ISSN:
0014-5793
,
1873-3468
DOI:
10.1016/S0014-5793(01)02730-2
Language:
English
Publisher:
Wiley
Publication Date:
2001
detail.hit.zdb_id:
1460391-3
SSG:
12
Permalink