Abstract:
:We have set up a model system for familial amyotrophic lateral sclerosis (FALS) by transfecting human neuroblastoma cell line SH-SY5Y with plasmids directing constitutive expression of either wild-type human Cu,Zn superoxide dismutase (Cu,ZnSOD) or a mutant of this enzyme (G93A) associated with FALS. We have tested mitochondrial function and determined cytosolic Ca2+ concentration in control cells (untransfected) and in cells expressing either wild-type Cu,ZnSOD or G93A. We report that G93A induces a significant loss of mitochondrial membrane potential, an increased sensitivity toward valinomycin and a parallel increase in cytosolic Ca2+ concentration. The above phenomena are not related to total Cu,ZnSOD content and activity in the cell.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Carrì MT,Ferri A,Battistoni A,Famhy L,Gabbianelli R,Poccia F,Rotilio Gdoi
10.1016/s0014-5793(97)01051-xsubject
Has Abstractpub_date
1997-09-08 00:00:00pages
365-8issue
2eissn
0014-5793issn
1873-3468pii
S0014-5793(97)01051-Xjournal_volume
414pub_type
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