pubmed-article:11747990 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11747990 | lifeskim:mentions | umls-concept:C0007600 | lld:lifeskim |
pubmed-article:11747990 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:11747990 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:11747990 | lifeskim:mentions | umls-concept:C0040132 | lld:lifeskim |
pubmed-article:11747990 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
pubmed-article:11747990 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:11747990 | lifeskim:mentions | umls-concept:C0004204 | lld:lifeskim |
pubmed-article:11747990 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:11747990 | pubmed:dateCreated | 2001-12-18 | lld:pubmed |
pubmed-article:11747990 | pubmed:abstractText | In PC-Cl3 rat thyroid cell line, ATP and UTP provoked a transient increase in [Ca(2+)](i), followed by a lower sustained phase. Removal of extracellular Ca(2+) reduced the initial transient response and completely abolished the plateau phase. Thapsigargin (TG) caused a rapid rise in [Ca(2+)](i) and subsequent addition of ATP was without effect. The transitory activation of [Ca(2+)](i) was dose-dependently attenuated in cells pretreated with the specific inhibitor of phospholipase C (PLC), U73122. These data suggest that the ATP-stimulated increment of [Ca(2+)](i) required InsP(3) formation and binding to its specific receptors in Ca(2+) stores. Desensitisation was demonstrated with respect to the calcium response to ATP and UTP in Fura 2-loaded cells. Further studies were performed to investigate whether the effect of ATP on Ca(2+) entry into PC-Cl3 cells was via L-type voltage-dependent Ca(2+) channels (L-VDCC) and/or by the capacitative pathway. Nifedipine decreased ATP-induced increase on [Ca(2+)](i). Addition of 2 mM Ca(2+) induced a [Ca(2+)](i) rise after pretreatment of the cells with TG or with 100 microM ATP in Ca(2+)-free medium. These data indicate that Ca(2+) entry into PC-Cl3 stimulated with ATP occurs through both an L-VDCC and through a capacitative pathway. Using buffers with differing Na(+) concentrations, we found that the effects of ATP were dependent of extracellular Na(+), suggesting that a Na(+)/Ca(2+) exchange mechanism is also operative. These data suggest the existence, in PC-Cl3 cell line, of a P2Y purinergic receptor able to increase the [Ca(2+)](i) via PLC activation, Ca(2+) store depletion, capacitative Ca(2+) entry and L-VDCC activation. | lld:pubmed |
pubmed-article:11747990 | pubmed:language | eng | lld:pubmed |
pubmed-article:11747990 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11747990 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:11747990 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11747990 | pubmed:month | Jan | lld:pubmed |
pubmed-article:11747990 | pubmed:issn | 0898-6568 | lld:pubmed |
pubmed-article:11747990 | pubmed:author | pubmed-author:MarsiglianteS... | lld:pubmed |
pubmed-article:11747990 | pubmed:author | pubmed-author:EliaMaria... | lld:pubmed |
pubmed-article:11747990 | pubmed:author | pubmed-author:Di JesoBrunoB | lld:pubmed |
pubmed-article:11747990 | pubmed:author | pubmed-author:GrecoSimonaS | lld:pubmed |
pubmed-article:11747990 | pubmed:author | pubmed-author:MuscellaAnton... | lld:pubmed |
pubmed-article:11747990 | pubmed:author | pubmed-author:StorelliCarlo... | lld:pubmed |
pubmed-article:11747990 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11747990 | pubmed:volume | 14 | lld:pubmed |
pubmed-article:11747990 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11747990 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11747990 | pubmed:pagination | 61-7 | lld:pubmed |
pubmed-article:11747990 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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pubmed-article:11747990 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:11747990 | pubmed:articleTitle | Increase of [Ca(2+)](i) via activation of ATP receptors in PC-Cl3 rat thyroid cell line. | lld:pubmed |
pubmed-article:11747990 | pubmed:affiliation | Laboratory of Physiology, Department of Biology, University of Lecce, Lecce 73100, Italy. smarsi@ilenic.unile.it | lld:pubmed |
pubmed-article:11747990 | pubmed:publicationType | Journal Article | lld:pubmed |
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