Novel <i>KCND3</i> Variant Underlying Nonprogressive Congenital Ataxia or SCA19/22 Disrupt K<sub>V</sub>4.3 Protein Expression and K+ Currents with Variable Effects on Channel Properties

Novel <i>KCND3</i> Variant Underlying Nonprogressive Congenital Ataxia or SCA19/22 Disrupt K<sub>V</sub>4.3 Protein Expression and K+ Currents with Variable Effects on Channel Properties

<i>KCND3</i> encodes the voltage-gated potassium channel K<sub>V</sub>4.3 that is highly expressed in the cerebellum, where it regulates dendritic excitability and calcium influx. Loss-of-function K<sub>V</sub>4.3 mutations have been associated with dominant spino...

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Bibliographic Details
Main Authors: Ginevra Zanni, Chen-Tsung Hsiao, Ssu-Ju Fu, Chih-Yung Tang, Alessandro Capuano, Luca Bosco, Federica Graziola, Emanuele Bellacchio, Serenella Servidei, Guido Primiano, Bing-Wen Soong, Chung-Jiuan Jeng
Format: Article
Language:English
Published: MDPI AG 2021-05-01
Series:International Journal of Molecular Sciences
Subjects:
<i>KCND3</i>
Spinocerebellar Ataxia SCA19/22
Congenital Ataxia
K<sub>V</sub>4.3
Online Access:https://www.mdpi.com/1422-0067/22/9/4986

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https://www.mdpi.com/1422-0067/22/9/4986

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