| pubmed-article:11600673 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11600673 | lifeskim:mentions | umls-concept:C0030274 | lld:lifeskim |
| pubmed-article:11600673 | lifeskim:mentions | umls-concept:C0120465 | lld:lifeskim |
| pubmed-article:11600673 | lifeskim:mentions | umls-concept:C0033706 | lld:lifeskim |
| pubmed-article:11600673 | lifeskim:mentions | umls-concept:C1414685 | lld:lifeskim |
| pubmed-article:11600673 | lifeskim:mentions | umls-concept:C1424447 | lld:lifeskim |
| pubmed-article:11600673 | lifeskim:mentions | umls-concept:C0030685 | lld:lifeskim |
| pubmed-article:11600673 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:11600673 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
| pubmed-article:11600673 | lifeskim:mentions | umls-concept:C0680255 | lld:lifeskim |
| pubmed-article:11600673 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:11600673 | lifeskim:mentions | umls-concept:C0391871 | lld:lifeskim |
| pubmed-article:11600673 | lifeskim:mentions | umls-concept:C1283071 | lld:lifeskim |
| pubmed-article:11600673 | lifeskim:mentions | umls-concept:C1963578 | lld:lifeskim |
| pubmed-article:11600673 | pubmed:issue | Pt 2 | lld:pubmed |
| pubmed-article:11600673 | pubmed:dateCreated | 2001-10-15 | lld:pubmed |
| pubmed-article:11600673 | pubmed:abstractText | 1. The signal transduction pathway responsible for cAMP-dependent Ca2+-induced Ca2+ release (CICR) from endoplasmic reticulum Ca2+ stores was assessed in the insulin-secreting cell line INS-1. 2. CICR was triggered by the GLP-1 receptor agonist exendin-4, an effect mimicked by caffeine, Sp-cAMPS or forskolin. CICR required influx of Ca2+ through L-type voltage-dependent Ca2+ channels, and was blocked by treatment with nimodipine, thapsigargin, or ryanodine, but not by the IP3 receptor antagonist xestospongin C. 3. Treatment with the cAMP antagonist 8-Br-Rp-cAMPS blocked CICR in response to exendin-4, whereas the PKA inhibitor H-89 was ineffective when tested at a concentration demonstrated to inhibit PKA-dependent gene expression. 4. RT-PCR of INS-1 cells demonstrated expression of mRNA coding for the type-II isoform of cAMP-regulated guanine nucleotide exchange factor (cAMP-GEF-II, Epac2). 5. CICR in response to forskolin was blocked by transient transfection and expression of a dominant negative mutant isoform of cAMP-GEF-II in which inactivating mutations were introduced into the exchange factor's two cAMP-binding domains. 6. It is concluded that CICR in INS-1 cells results from GLP-1 receptor-mediated sensitization of the intracellular Ca2+ release mechanism, a signal transduction pathway independent of PKA, but which requires cAMP-GEF-II. | lld:pubmed |
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| pubmed-article:11600673 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11600673 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11600673 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11600673 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11600673 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11600673 | pubmed:status | MEDLINE | lld:pubmed |
