pubmed-article:15632122 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15632122 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
pubmed-article:15632122 | lifeskim:mentions | umls-concept:C0001492 | lld:lifeskim |
pubmed-article:15632122 | lifeskim:mentions | umls-concept:C0021547 | lld:lifeskim |
pubmed-article:15632122 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
pubmed-article:15632122 | lifeskim:mentions | umls-concept:C0030685 | lld:lifeskim |
pubmed-article:15632122 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
pubmed-article:15632122 | lifeskim:mentions | umls-concept:C0680255 | lld:lifeskim |
pubmed-article:15632122 | lifeskim:mentions | umls-concept:C0391871 | lld:lifeskim |
pubmed-article:15632122 | lifeskim:mentions | umls-concept:C1283071 | lld:lifeskim |
pubmed-article:15632122 | lifeskim:mentions | umls-concept:C1963578 | lld:lifeskim |
pubmed-article:15632122 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
pubmed-article:15632122 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:15632122 | pubmed:dateCreated | 2005-3-7 | lld:pubmed |
pubmed-article:15632122 | pubmed:abstractText | In A7r5 smooth muscle cells, vasopressin stimulates release of Ca2+ from intracellular stores and Ca2+ entry, and it inhibits adenylyl cyclase (AC) activity. Inhibition of AC is prevented by inhibition of phospholipase C or when the increase in cytosolic [Ca2+] is prevented by the Ca2+ buffer, BAPTA. It is unaffected by pertussis toxin, inhibition of protein kinase C, or L-type Ca2+ channels or by removal of extracellular Ca2+. The independence of extracellular Ca2+ occurs despite inhibition of AC by vasopressin persisting for at least 15 min, whereas the cytosolic [Ca2+] returns to its basal level within 1-2 min in Ca2+-free medium. Although capacitative Ca2+ entry (CCE), activated by emptying stores with thapsigargin, inhibits AC, Ca2+ entry via CCE or L-type Ca2+ channels activated by vasopressin is ineffective. Temporally separating vasopressin-evoked Ca2+ release from the assessment of AC activity revealed that the transient Ca2+ signal resulting from Ca2+ mobilization causes a long lasting inhibition of AC. By contrast, inhibition of AC by thapsigargin-evoked CCE reverses rapidly after removal of extracellular Ca2+. Inhibition of AC by vasopressin is prevented by inhibition of Ca2+-calmodulin-dependent protein kinase II. We conclude that persistent inhibition of AC (probably AC-3) by vasopressin is mediated by inositol trisphosphate-evoked Ca2+ release causing activation of Ca2+-calmodulin-dependent protein kinase II. Our results establish that an important interaction between two ubiquitous signaling pathways is tuned selectively to Ca2+ release via inositol trisphosphate receptors and that the interaction transduces a transient Ca2+ signal into a long lasting inhibition of AC. | lld:pubmed |
pubmed-article:15632122 | pubmed:language | eng | lld:pubmed |
pubmed-article:15632122 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15632122 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:15632122 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15632122 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15632122 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15632122 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15632122 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15632122 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15632122 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15632122 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15632122 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15632122 | pubmed:month | Mar | lld:pubmed |
pubmed-article:15632122 | pubmed:issn | 0021-9258 | lld:pubmed |
pubmed-article:15632122 | pubmed:author | pubmed-author:TaylorColin... | lld:pubmed |
pubmed-article:15632122 | pubmed:author | pubmed-author:LiuYingjieY | lld:pubmed |
pubmed-article:15632122 | pubmed:author | pubmed-author:DyerJeanette... | lld:pubmed |
pubmed-article:15632122 | pubmed:author | pubmed-author:de la... | lld:pubmed |
pubmed-article:15632122 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15632122 | pubmed:day | 11 | lld:pubmed |
pubmed-article:15632122 | pubmed:volume | 280 | lld:pubmed |
pubmed-article:15632122 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15632122 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15632122 | pubmed:pagination | 8936-44 | lld:pubmed |
pubmed-article:15632122 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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pubmed-article:15632122 | pubmed:meshHeading | pubmed-meshheading:15632122... | lld:pubmed |
pubmed-article:15632122 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:15632122 | pubmed:articleTitle | Long lasting inhibition of adenylyl cyclase selectively mediated by inositol 1,4,5-trisphosphate-evoked calcium release. | lld:pubmed |
pubmed-article:15632122 | pubmed:affiliation | Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1PD, United Kingdom. | lld:pubmed |
pubmed-article:15632122 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15632122 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:15632122 | lld:pubmed |