rdf:type |
|
lifeskim:mentions |
umls-concept:C0009368,
umls-concept:C0025914,
umls-concept:C0026809,
umls-concept:C0035820,
umls-concept:C0036536,
umls-concept:C0036537,
umls-concept:C0439799,
umls-concept:C0596019,
umls-concept:C1416602,
umls-concept:C1416611,
umls-concept:C1416612,
umls-concept:C2697834
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pubmed:issue |
3
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pubmed:dateCreated |
2007-2-19
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pubmed:abstractText |
Colonic crypts are the site of Cl- secretion. Basolateral K+ channels provide the driving force for luminal cystic fibrosis transmembrane regulator-mediated Cl- exit. Relevant colonic epithelial K+ channels are the intermediate conductance Ca2+-activated K(Ca)3.1 (SK4) channel and the cAMP-activated K(V)7.1 (KCNQ1) channel. In addition, big conductance Ca2+-activated K(Ca)1.1 (BK) channels may play a role in Ca2+-activated Cl- secretion. Here we use K(Ca)1.1 and K(Ca)3.1 knock-out mice, and the K(V)7.1 channel inhibitor 293B (10 microm) to investigate the role of K(Ca)1.1, K(Ca)3.1 and K(V)7.1 channels in cholinergic-stimulated Cl- secretion.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/6-cyano-4-(N-ethylsulfonyl-N-methyla...,
http://linkedlifedata.com/resource/pubmed/chemical/Carbachol,
http://linkedlifedata.com/resource/pubmed/chemical/Chlorides,
http://linkedlifedata.com/resource/pubmed/chemical/Cholinergic Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Chromans,
http://linkedlifedata.com/resource/pubmed/chemical/Forskolin,
http://linkedlifedata.com/resource/pubmed/chemical/Intermediate-Conductance...,
http://linkedlifedata.com/resource/pubmed/chemical/KCNQ1 Potassium Channel,
http://linkedlifedata.com/resource/pubmed/chemical/Kcnn4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Large-Conductance...,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfonamides
|
pubmed:status |
MEDLINE
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pubmed:month |
Mar
|
pubmed:issn |
1748-1708
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
189
|
pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
|
pubmed:pagination |
251-8
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pubmed:dateRevised |
2009-2-3
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pubmed:meshHeading |
pubmed-meshheading:17305705-Animals,
pubmed-meshheading:17305705-Carbachol,
pubmed-meshheading:17305705-Chlorides,
pubmed-meshheading:17305705-Cholinergic Agonists,
pubmed-meshheading:17305705-Chromans,
pubmed-meshheading:17305705-Colon,
pubmed-meshheading:17305705-Female,
pubmed-meshheading:17305705-Forskolin,
pubmed-meshheading:17305705-Intermediate-Conductance Calcium-Activated Potassium...,
pubmed-meshheading:17305705-Intestinal Mucosa,
pubmed-meshheading:17305705-KCNQ1 Potassium Channel,
pubmed-meshheading:17305705-Large-Conductance Calcium-Activated Potassium Channels,
pubmed-meshheading:17305705-Male,
pubmed-meshheading:17305705-Mice,
pubmed-meshheading:17305705-Mice, Inbred C57BL,
pubmed-meshheading:17305705-Mice, Knockout,
pubmed-meshheading:17305705-Potassium Channel Blockers,
pubmed-meshheading:17305705-Potassium Channels,
pubmed-meshheading:17305705-Random Allocation,
pubmed-meshheading:17305705-Sulfonamides
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pubmed:year |
2007
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pubmed:articleTitle |
Role of cholinergic-activated KCa1.1 (BK), KCa3.1 (SK4) and KV7.1 (KCNQ1) channels in mouse colonic Cl- secretion.
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pubmed:affiliation |
Institute of Physiology and Biophysics, The Water and Salt Research Center, University of Aarhus, Aarhus C, Denmark.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|