Linked Life Data

20712895

Source:http://linkedlifedata.com/resource/pubmed/id/20712895

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2010-9-6
pubmed:abstractText
The zebrafish has been suggested as a model system for studying human diseases that affect nervous system function and motor output. However, few of the ion channels that control neuronal activity in zebrafish have been characterized. Here, we have identified zebrafish orthologs of voltage-dependent Kv3 (KCNC) K+ channels. Kv3 channels have specialized gating properties that facilitate high-frequency, repetitive firing in fast-spiking neurons. Mutations in human Kv3.3 cause spinocerebellar ataxia type 13 (SCA13), an autosomal dominant genetic disease that exists in distinct neurodevelopmental and neurodegenerative forms. To assess the potential usefulness of the zebrafish as a model system for SCA13, we have characterized the functional properties of zebrafish Kv3.3 channels with and without mutations analogous to those that cause SCA13.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1471-2202
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
99
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Functional effects of spinocerebellar ataxia type 13 mutations are conserved in zebrafish Kv3.3 channels.
pubmed:affiliation
Department of Physiology David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095-1751 USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural