pubmed-article:11696608 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11696608 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
pubmed-article:11696608 | lifeskim:mentions | umls-concept:C0243192 | lld:lifeskim |
pubmed-article:11696608 | lifeskim:mentions | umls-concept:C2003941 | lld:lifeskim |
pubmed-article:11696608 | lifeskim:mentions | umls-concept:C0279023 | lld:lifeskim |
pubmed-article:11696608 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
pubmed-article:11696608 | lifeskim:mentions | umls-concept:C1709305 | lld:lifeskim |
pubmed-article:11696608 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
pubmed-article:11696608 | lifeskim:mentions | umls-concept:C0442821 | lld:lifeskim |
pubmed-article:11696608 | lifeskim:mentions | umls-concept:C0220821 | lld:lifeskim |
pubmed-article:11696608 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:11696608 | pubmed:dateCreated | 2001-11-6 | lld:pubmed |
pubmed-article:11696608 | pubmed:abstractText | A defining property of L-type Ca(2+) channels is their potentiation by both 1,4-dihydropyridine agonists and strong depolarization. In contrast, non-L-type channels are potentiated by neither agonist nor depolarization, suggesting that these two processes may by linked. In this study, we have tested whether the mechanisms of agonist- and depolarization-induced potentiation in the cardiac L-type channel (alpha(1C)) are linked. We found that the mutant L-type channel GFP-alpha(1C)(TQ-->YM), bearing the mutations T1066Y and Q1070M, was able to undergo depolarization-induced potentiation but not potentiation by agonist. Conversely, the chimeric channel GFP-CACC was potentiated by agonist but not by strong depolarization. These data indicate that the mechanisms of agonist- and depolarization-induced potentiation of alpha(1C) are distinct. Since neither GFP-CACC nor GFP-CCAA was potentiated significantly by depolarization, no single repeat of alpha(1C) appears to be responsible for depolarization-induced potentiation. Surprisingly, GFP-CACC displayed a low estimated open probability similar to that of the alpha(1C), but could not support depolarization-induced potentiation, demonstrating that a relatively low open probability alone is not sufficient for depolarization-induced potentiation to occur. Thus, depolarization-induced potentiation may be a global channel property requiring participation from all four homologous repeats. | lld:pubmed |
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pubmed-article:11696608 | pubmed:language | eng | lld:pubmed |
pubmed-article:11696608 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11696608 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11696608 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11696608 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:11696608 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11696608 | pubmed:month | Nov | lld:pubmed |
pubmed-article:11696608 | pubmed:issn | 0022-1295 | lld:pubmed |
pubmed-article:11696608 | pubmed:author | pubmed-author:BeamK GKG | lld:pubmed |
pubmed-article:11696608 | pubmed:author | pubmed-author:GrabnerMM | lld:pubmed |
pubmed-article:11696608 | pubmed:author | pubmed-author:WilkensC MCM | lld:pubmed |
pubmed-article:11696608 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11696608 | pubmed:volume | 118 | lld:pubmed |
pubmed-article:11696608 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11696608 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11696608 | pubmed:pagination | 495-508 | lld:pubmed |
pubmed-article:11696608 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:11696608 | pubmed:meshHeading | pubmed-meshheading:11696608... | lld:pubmed |
pubmed-article:11696608 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11696608 | pubmed:articleTitle | Potentiation of the cardiac L-type Ca(2+) channel (alpha(1C)) by dihydropyridine agonist and strong depolarization occur via distinct mechanisms. | lld:pubmed |
pubmed-article:11696608 | pubmed:affiliation | Department of Anatomy and Neurobiology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA. | lld:pubmed |
pubmed-article:11696608 | pubmed:publicationType | Journal Article | lld:pubmed |