Tryptophan 32 mediates SOD1 toxicity in a in vivo motor neuron model of ALS and is a promising target for small molecule therapeutics

Tryptophan 32 mediates SOD1 toxicity in a in vivo motor neuron model of ALS and is a promising target for small molecule therapeutics

SOD1 misfolding, toxic gain of function, and spread are proposed as a pathological basis of amyotrophic lateral sclerosis (ALS), but the nature of SOD1 toxicity has been difficult to elucidate. Uniquely in SOD1 proteins from humans and other primates, and rarely in other species, a tryptophan residu...

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Bibliographic Details
Main Authors: Michèle G. DuVal, Vijaya K. Hinge, Natalie Snyder, Richard Kanyo, Jenna Bratvold, Edward Pokrishevsky, Neil R. Cashman, Nikolay Blinov, Andriy Kovalenko, W. Ted Allison
Format: Article
Language:English
Published: Elsevier 2019-04-01
Series:Neurobiology of Disease
Subjects:
[Cu-Zn] superoxide dismutase 1
Protein misfolding
Prion-like disease
Neuromuscular disease
Amyotrophic lateral sclerosis
Zebrafish
Online Access:http://www.sciencedirect.com/science/article/pii/S0969996118307551

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