Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
1994-5-6
|
| pubmed:abstractText |
The receptor-mediated agonist, neurotensin (NT) stimulated Ba(2+)- and charybdotoxin-sensitive 86Rb (K+) efflux in the HT29-19A colonic cell line. Efflux was also stimulated by ionomycin and thapsigargin and could be abolished by incubation with the intracellular Ca2+ chelator, BAPTA. Together, these data suggest a rise in [Ca2+]i is prerequisite for activation of K+ efflux in these cells. Comparison of the temporal profiles for NT-induced increases in [Ca2+]i and 86Rb efflux, however, failed to show a direct relationship between these parameters. The NT-stimulated increase in [Ca2+]i was transient, returning to baseline within 4-5 min, while efflux was sustained over a much longer period (> 12 min). Ca(2+)-activated 86Rb efflux was inhibited by pretreatment with calmodulin (CaM) antagonist, W7. W7 had no effect on basal efflux, but reduced both NT- and IM-activated efflux up to 80%, with a Ki of 38 microM. Other CaM antagonist inhibited efflux with an order of potency (TFP approximately W8 > W7 >> W5) consistent with inhibition of a CaM-dependent process. Inhibition by W7 was not abolished by ouabain or bumetanide, indicating its effects are not mediated by action upon K+ uptake processes. W7 did not inhibit NT-stimulated 125I efflux but significantly reduced efflux stimulated by the Ca2+ ionophore, ionomycin. NT-stimulated 86Rb+ efflux was localized to the basolateral membrane of HT29-19A monolayers grown on permeable supports. These data are consistent with the involvement of CaM in mediating Ca(2+)-dependent activation of K+ conductance in HT29-19A colonocytes.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1,2-bis(2-aminophenoxy)ethane-N,N,N'...,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calmodulin,
http://linkedlifedata.com/resource/pubmed/chemical/Chloride Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Egtazic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Iodine Radioisotopes,
http://linkedlifedata.com/resource/pubmed/chemical/Ionomycin,
http://linkedlifedata.com/resource/pubmed/chemical/Neurotensin,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Rubidium Radioisotopes,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfonamides,
http://linkedlifedata.com/resource/pubmed/chemical/W 7
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0006-3002
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
31
|
| pubmed:volume |
1221
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
185-92
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:8148397-Calcium,
pubmed-meshheading:8148397-Calmodulin,
pubmed-meshheading:8148397-Cell Line,
pubmed-meshheading:8148397-Chloride Channels,
pubmed-meshheading:8148397-Colon,
pubmed-meshheading:8148397-Egtazic Acid,
pubmed-meshheading:8148397-Humans,
pubmed-meshheading:8148397-Iodine Radioisotopes,
pubmed-meshheading:8148397-Ionomycin,
pubmed-meshheading:8148397-Neurotensin,
pubmed-meshheading:8148397-Potassium Channels,
pubmed-meshheading:8148397-Rubidium Radioisotopes,
pubmed-meshheading:8148397-Sulfonamides
|
| pubmed:year |
1994
|
| pubmed:articleTitle |
Involvement of calmodulin in Ca(2+)-activated K+ efflux in human colonic cell line, HT29-19A.
|
| pubmed:affiliation |
Epithelial Membrane Research Centre, University of Manchester, Hope Hospital, Salford, UK.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|