Cerebellar ataxia and Purkinje cell dysfunction caused by Ca2+-activated K+ channel deficiency-Reference-Cited by-同舟云学术

Cerebellar ataxia and Purkinje cell dysfunction caused by Ca2+-activated K+ channel deficiency

Published:2004-06-11 Issue:25 Volume:101 Page:9474-9478
ISSN:0027-8424
Container-title:Proceedings of the National Academy of Sciences
language:en
Short-container-title:Proceedings of the National Academy of Sciences

Author:

Sausbier M.,Hu H.,Arntz C.,Feil S.,Kamm S.,Adelsberger H.,Sausbier U.,Sailer C. A.,Feil R.,Hofmann F.,Korth M.,Shipston M. J.,Knaus H.-G.,Wolfer D. P.,Pedroarena C. M.,Storm J. F.,Ruth P.

Publisher

Proceedings of the National Academy of Sciences

Subject

Multidisciplinary

Reference39 articles.

1. Ion channel genes and human neurological disease: Recent progress, prospects, and challenges

2. Episodic ataxia/myokymia syndrome is associated with point mutations in the human potassium channel gene, KCNA1

3. A mouse model of episodic ataxia type-1

4. A novel potassium channel gene, KCNQ2, is mutated in an inherited epilepsy of newborns

5. The weaver mutation of GIRK2 results in a loss of inwardly rectifying K+ current in cerebellar granule cells.

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