TorsinB overexpression prevents abnormal twisting in DYT1 dystonia mouse models

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...

Ausführliche Beschreibung

Bibliographische Detailangaben
Hauptverfasser: Jay Li, Chun-Chi Liang, Samuel S Pappas, William T Dauer
Format: Artikel
Sprache:English
Veröffentlicht: eLife Sciences Publications Ltd 2020-03-01
Schriftenreihe:eLife
Schlagworte:
dystonia
mouse model
genetic redundancy
movement disorder
basal ganglia
cholinergic interneuron
Online Zugang:https://elifesciences.org/articles/54285

Online

https://elifesciences.org/articles/54285

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