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  Respiration and parturition affected by conditional overexpression of the Ca2+-activated K+ channel subunit, SK3.

Bond, C. T., Sprengel, R., Bissonnette, J. M., Kaufmann, W. A., Pribnow, D., Neelands, T., et al. (2000). Respiration and parturition affected by conditional overexpression of the Ca2+-activated K+ channel subunit, SK3. Science, 289(5486), 1942-1946. doi:10.1126/science.289.5486.1942.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0028-2CB9-0 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0028-2CBA-E
Genre: Journal Article
Alternative Title : Respiration and parturition affected by conditional overexpression of the Ca2+-activated K+ channel subunit, SK3.

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Science_289_2000_1942.pdf (Any fulltext), 380KB
 
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Bond, Chris T., Author
Sprengel, Rolf1, Author              
Bissonnette, John M., Author
Kaufmann, Walter A., Author
Pribnow, David, Author
Neelands, Torben, Author
Storck, Thorsten, Author
Baetscher, Manfred, Author
Jerecic, Jasna1, Author              
Maylie, James, Author
Knaus, Hans−Günther, Author
Seeburg, Peter H.1, Author              
Adelman, John P., Author
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1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              

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 Abstract: In excitable cells, small-conductance Ca2+-activated potassium channels (SK channels) are responsible for the slow after-hyperpolarization that often follows an action potential. Three SK channel subunits have been molecularly characterized. The SK3 gene was targeted by homologous recombination for the insertion of a gene switch that permitted experimental regulation of SK3 expression while retaining normal SK3 promoter function. An absence of SK3 did not present overt phenotypic consequences. However, SK3 overexpression induced abnormal respiratory responses to hypoxia and compromised parturition. Both conditions were corrected by silencing the gene. The results implicate SK3 channels as potential therapeutic targets for disorders such as sleep apnea or sudden infant death syndrome and for regulating uterine contractions during labor.

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Language(s): eng - English
 Dates: 2000-07-212000-09-15
 Publication Status: Published in print
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 Rev. Type: Peer
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Title: Science
Source Genre: Journal
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Publ. Info: Washington, D.C. : American Association for the Advancement of Science
Pages: - Volume / Issue: 289 (5486) Sequence Number: - Start / End Page: 1942 - 1946 Identifier: ISSN: 0036-8075
CoNE: https://pure.mpg.de/cone/journals/resource/991042748276600_1