Source:http://linkedlifedata.com/resource/pubmed/id/10936215
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2000-9-12
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| pubmed:abstractText |
The Drosophila slowpoke gene encodes a large conductance calcium-activated potassium channel used in neurons, muscle, and some epithelial cells. Tissue-specific transcriptional promoters and alternative mRNA splicing generate a large array of transcripts. These distinct transcripts are thought to tailor the properties of the channel to the requirements of the cell. Presumably, a single splice variant cannot satisfy the specific needs of all cell types. To test this, we examined whether a single slowpoke splice variant was capable of complementing all slowpoke behavioral phenotypes. Null mutations in slowpoke cause animals to be semiflightless and to manifest an inducible "sticky-feet" phenotype. The well-characterized slowpoke transcriptional control region was used to direct the expression of a single slowpoke splice variant (cDNA H13) in transgenic flies. The endogenous gene in these flies had been inactivated by the slo(4) mutation. Action-potential recordings and voltage-clamp recordings demonstrated the production of functional channels from the transgene. The transgene completely complemented the flight defect, but not the sticky-feet phenotype. We conclude that distinct slowpoke channel isoforms, produced by alternative splicing, are not interchangeable and are required for proper function of different cell types.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Drosophila Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Large-Conductance...,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels...,
http://linkedlifedata.com/resource/pubmed/chemical/slo protein, Drosophila
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| pubmed:status |
MEDLINE
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| pubmed:month |
Sep
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| pubmed:issn |
0022-3042
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
75
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1310-9
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:10936215-Action Potentials,
pubmed-meshheading:10936215-Alternative Splicing,
pubmed-meshheading:10936215-Amino Acid Sequence,
pubmed-meshheading:10936215-Animals,
pubmed-meshheading:10936215-Animals, Genetically Modified,
pubmed-meshheading:10936215-Drosophila,
pubmed-meshheading:10936215-Drosophila Proteins,
pubmed-meshheading:10936215-Exons,
pubmed-meshheading:10936215-Flight, Animal,
pubmed-meshheading:10936215-Genetic Complementation Test,
pubmed-meshheading:10936215-Genetic Variation,
pubmed-meshheading:10936215-Large-Conductance Calcium-Activated Potassium Channels,
pubmed-meshheading:10936215-Models, Molecular,
pubmed-meshheading:10936215-Molecular Sequence Data,
pubmed-meshheading:10936215-Muscle, Skeletal,
pubmed-meshheading:10936215-Potassium Channels,
pubmed-meshheading:10936215-Potassium Channels, Calcium-Activated,
pubmed-meshheading:10936215-Promoter Regions, Genetic,
pubmed-meshheading:10936215-Protein Structure, Secondary,
pubmed-meshheading:10936215-Transcription, Genetic
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| pubmed:year |
2000
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| pubmed:articleTitle |
Complementation of physiological and behavioral defects by a slowpoke Ca(2+) -activated K(+) channel transgene.
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| pubmed:affiliation |
Section of Neurobiology and the Institute for Cellular and Molecular Biology, The University of Texas at Austin, 78712-1064, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.
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