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Article

Aggregation-triggering segments of SOD1 fibril formation support a common pathway for familial and sporadic ALS.

Proceedings of the National Academy of Sciences of the United States of America - 7 Jan 2014

Ivanova Magdalena I, Sievers Stuart A, Guenther Elizabeth L, Johnson Lisa M, Winkler Duane D, Galaleldeen Ahmad, Sawaya Michael R, Hart P John, Eisenberg David S

Abstract excerpt

ALS is a terminal disease of motor neurons that is characterized by accumulation of proteinaceous deposits in affected cells. Pathological deposition of mutated Cu/Zn superoxide dismutase (SOD1) accounts for ∼20% of the familial ALS (fALS) cases. However, understanding the molecular link between mutation and disease has been difficult, given that more than 140 different SOD1 mutants have been observed in fALS...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 24344300
DOI: 10.1073/pnas.1320786110
PMCID: PMC3890817

Genes

SOD1

Provenance

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