| pubmed-article:7798198 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7798198 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
| pubmed-article:7798198 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:7798198 | lifeskim:mentions | umls-concept:C1515877 | lld:lifeskim |
| pubmed-article:7798198 | lifeskim:mentions | umls-concept:C1698986 | lld:lifeskim |
| pubmed-article:7798198 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
| pubmed-article:7798198 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:7798198 | lifeskim:mentions | umls-concept:C0333668 | lld:lifeskim |
| pubmed-article:7798198 | pubmed:issue | 51 | lld:pubmed |
| pubmed-article:7798198 | pubmed:dateCreated | 1995-1-24 | lld:pubmed |
| pubmed-article:7798198 | pubmed:abstractText | Glucose stimulation of beta-cell insulin secretion is initiated by membrane depolarization coupled with an elevation in intracellular Ca2+ concentration ([Ca2+]i). Both depolarization-dependent Ca2+ entry and intracellular Ca2+ store release contribute to the sugar-induced rise in [Ca2+]i. Here we show that maneuvers depleting intracellular Ca2+ stores induce membrane depolarization and a sustained nitrendipine-sensitive Ca2+ influx, whereas interventions promoting Ca2+ store refilling produce a hyperpolarization and inhibit Ca2+ influx. Both intracellular Ca2+ store depletion and maitotoxin activated a depolarizing nonselective cation current carried principally by Na+ in the physiological range of membrane potentials. The activation of such a current may form the paradigm by which excitable cells refill depleted intracellular Ca2+ stores by depolarization-driven opening of voltage-activated Ca2+ channels. | lld:pubmed |
| pubmed-article:7798198 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7798198 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7798198 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:7798198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7798198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7798198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7798198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7798198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7798198 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7798198 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:7798198 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:7798198 | pubmed:author | pubmed-author:SpencerBB | lld:pubmed |
| pubmed-article:7798198 | pubmed:author | pubmed-author:WorleyJ... | lld:pubmed |
| pubmed-article:7798198 | pubmed:author | pubmed-author:DukesI DID | lld:pubmed |
| pubmed-article:7798198 | pubmed:author | pubmed-author:McIntyreM SMS | lld:pubmed |
| pubmed-article:7798198 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7798198 | pubmed:day | 23 | lld:pubmed |
| pubmed-article:7798198 | pubmed:volume | 269 | lld:pubmed |
| pubmed-article:7798198 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7798198 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7798198 | pubmed:pagination | 32055-8 | lld:pubmed |
| pubmed-article:7798198 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:7798198 | pubmed:meshHeading | pubmed-meshheading:7798198-... | lld:pubmed |
| pubmed-article:7798198 | pubmed:meshHeading | pubmed-meshheading:7798198-... | lld:pubmed |
| pubmed-article:7798198 | pubmed:meshHeading | pubmed-meshheading:7798198-... | lld:pubmed |
| pubmed-article:7798198 | pubmed:meshHeading | pubmed-meshheading:7798198-... | lld:pubmed |
| pubmed-article:7798198 | pubmed:meshHeading | pubmed-meshheading:7798198-... | lld:pubmed |
| pubmed-article:7798198 | pubmed:meshHeading | pubmed-meshheading:7798198-... | lld:pubmed |
| pubmed-article:7798198 | pubmed:meshHeading | pubmed-meshheading:7798198-... | lld:pubmed |
| pubmed-article:7798198 | pubmed:meshHeading | pubmed-meshheading:7798198-... | lld:pubmed |
| pubmed-article:7798198 | pubmed:meshHeading | pubmed-meshheading:7798198-... | lld:pubmed |
| pubmed-article:7798198 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7798198 | pubmed:articleTitle | Depletion of intracellular Ca2+ stores activates a maitotoxin-sensitive nonselective cationic current in beta-cells. | lld:pubmed |
| pubmed-article:7798198 | pubmed:affiliation | Department of Cell Physiology, Glaxo Research Institute, Research Triangle Park, North Carolina 27709. | lld:pubmed |
| pubmed-article:7798198 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7798198 | pubmed:publicationType | In Vitro | lld:pubmed |
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