Mutant SOD1 forms ion channel: Implications for ALS pathophysiology

Mutant SOD1 forms ion channel: Implications for ALS pathophysiology

Point mutations in the gene encoding copper–zinc superoxide dismutase (SOD1) impart a gain-of-function to this protein that underlies 20–25% of all familial amyotrophic lateral sclerosis (FALS) cases. However, the specific mechanism of mutant SOD1 toxicity has remained elusive. Using the complementa...

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Bibliographic Details
Main Authors: Michael J. Allen, Jérome J. Lacroix, Srinivasan Ramachandran, Ricardo Capone, Jenny L. Whitlock, Ghanashyam D. Ghadge, Morton F. Arnsdorf, Raymond P. Roos, Ratnesh Lal
Format: Article
Language:English
Published: Elsevier 2012-03-01
Series:Neurobiology of Disease
Subjects:
Amyotrophic lateral sclerosis
Superoxide dismutase
A4V
Protein misfolding
Atomic force microscopy
Fluo-4 calcium assay
Online Access:http://www.sciencedirect.com/science/article/pii/S096999611100297X

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http://www.sciencedirect.com/science/article/pii/S096999611100297X

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