TorsinB overexpression prevents abnormal twisting in DYT1 dystonia mouse models

Genetic redundancy can be exploited to identify therapeutic targets for inherited disorders. We explored this possibility in DYT1 dystonia, a neurodevelopmental movement disorder caused by a loss-of-function (LOF) mutation in the TOR1A gene encoding torsinA. Prior work demonstrates that torsinA and...

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Bibliographic Details
Published in:eLife
Main Authors: Jay Li, Chun-Chi Liang, Samuel S Pappas, William T Dauer
Format: Article
Language:English
Published: eLife Sciences Publications Ltd 2020-03-01
Subjects:
dystonia
mouse model
genetic redundancy
movement disorder
basal ganglia
cholinergic interneuron
Online Access:https://elifesciences.org/articles/54285

Internet

https://elifesciences.org/articles/54285

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