| pubmed-article:17938170 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17938170 | lifeskim:mentions | umls-concept:C0036536 | lld:lifeskim |
| pubmed-article:17938170 | lifeskim:mentions | umls-concept:C0036537 | lld:lifeskim |
| pubmed-article:17938170 | lifeskim:mentions | umls-concept:C1325604 | lld:lifeskim |
| pubmed-article:17938170 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:17938170 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:17938170 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:17938170 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:17938170 | pubmed:dateCreated | 2007-12-31 | lld:pubmed |
| pubmed-article:17938170 | pubmed:abstractText | Non-hydrolyzable GTP analogues, such as guanosine 5'-(beta, gamma-imido)triphosphate (GppNHp), induce granule secretion from permeabilized platelets in the absence of increased intracellular Ca(2+). Here, we show that the GppNHp-induced dense granule secretion from permeabilized platelets occurred concomitantly with the activation of small GTPase Ral. This secretion was inhibited by the addition of GTP-Ral-binding domain (RBD) of Sec5, which is a component of the exocyst complex known to function as a tethering factor at the plasma membrane for vesicles. We generated an antibody against Sec5-RBD, which abolished the interaction between GTP-Ral and the exocyst complex in vitro. The addition of this antibody inhibited the GppNHp-induced secretion. These data indicate that Ral mediates the GppNHp-induced dense granule secretion from permeabilized platelets through interaction with its effector, the exocyst complex. Furthermore, GppNHp enhanced the Ca(2+) sensitivity of dense granule secretion from permeabilized platelets, and this enhancement was inhibited by Sec5-RBD. In intact platelets, the association between Ral and the exocyst complex was induced by thrombin stimulation with a time course similar to that of dense granule secretion and Ral activation. Taken together, our results suggest that the Ral-exocyst pathway participates in the regulation of platelet dense granule secretion by enhancing the Ca(2+) sensitivity of the secretion. | lld:pubmed |
| pubmed-article:17938170 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17938170 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17938170 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17938170 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17938170 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17938170 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17938170 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17938170 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17938170 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17938170 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17938170 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17938170 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17938170 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:17938170 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:17938170 | pubmed:author | pubmed-author:OkawaKatsuyaK | lld:pubmed |
| pubmed-article:17938170 | pubmed:author | pubmed-author:KitaToruT | lld:pubmed |
| pubmed-article:17938170 | pubmed:author | pubmed-author:FukaiShuyaS | lld:pubmed |
| pubmed-article:17938170 | pubmed:author | pubmed-author:NurekiOsamuO | lld:pubmed |
| pubmed-article:17938170 | pubmed:author | pubmed-author:HoriuchiHisan... | lld:pubmed |
| pubmed-article:17938170 | pubmed:author | pubmed-author:KondoHirokazu... | lld:pubmed |
| pubmed-article:17938170 | pubmed:author | pubmed-author:HigashiTomohi... | lld:pubmed |
| pubmed-article:17938170 | pubmed:author | pubmed-author:ShirakawaRyut... | lld:pubmed |
| pubmed-article:17938170 | pubmed:author | pubmed-author:IkedaTomoyuki... | lld:pubmed |
| pubmed-article:17938170 | pubmed:author | pubmed-author:KawatoMitsuno... | lld:pubmed |
| pubmed-article:17938170 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17938170 | pubmed:day | 4 | lld:pubmed |
| pubmed-article:17938170 | pubmed:volume | 283 | lld:pubmed |
| pubmed-article:17938170 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17938170 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17938170 | pubmed:pagination | 166-74 | lld:pubmed |
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| pubmed-article:17938170 | pubmed:meshHeading | pubmed-meshheading:17938170... | lld:pubmed |
| pubmed-article:17938170 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:17938170 | pubmed:articleTitle | Regulation of platelet dense granule secretion by the Ral GTPase-exocyst pathway. | lld:pubmed |
| pubmed-article:17938170 | pubmed:affiliation | Department of Cardiovascular Medicine and Frontier Technology Center, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. | lld:pubmed |
| pubmed-article:17938170 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17938170 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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