@article{oai:miyazaki-u.repo.nii.ac.jp:00000268,
 author = {伊藤, 勝昭 and Ito, Katsuaki and 池田, 正浩 and Ikeda, Masahiro and Shiraishi, Mitsuya and Kawashima, Sachiko and Moroi, Masaaki and Shin, Yangchol and Morita, Takashi and Horii, Yoichiro and 伊藤, 勝昭 and Ito, Katsuaki},
 issue = {2},
 journal = {Thrombosis and Haemostasis},
 month = {},
 note = {Decreased platelet aggregation to collagen is a cause for bleeding diathesis of Chediak-Higashi syndrome (CHS). We investigated whether the collagen receptor - Ca2+ signaling system was impaired in platelets from cattle affected with CHS. Collagen-induced increase in cytosolic Ca2+ ([Ca2+]i) was depressed in CHS platelets, which was accompanied by a decrease in production of inositol 1,4,5-trisphosphate. Under the condition that influences of endogenous arachidonic acid metabolites and ADP were excluded, convulxin or collagen-related peptide, which are specific agonists for the collagen receptor GPVI, increased [Ca2+]i similarly in normal and CHS platelets. In contrast, rhodocytin, which was proposed to activate another collagen receptor GPIa/IIa, increased [Ca2+]i much less in CHS platelets than in normal ones. Cytochalasin D, an actin polymerization inhibitor, depressed the response to collagen or rhodocytin but not that to convulxin. Adhesion of CHS platelets to acid soluble type I collagen, which was mediated by GPIa/IIa, was similar to that of normal platelets. These results suggest that a defect in rhodocytin-sensitive pathway is responsible for depression of response to collagen in CHS platelets. It remains to be determined what receptor is associated with the mechanism.},
 pages = {334--341},
 title = {A Defect in Collagen Receptor-Ca2+ Signaling System in Platelets from Cattle with Chediak-Higashi Syndrome},
 volume = {87},
 year = {2002},
 yomi = {イトウ, カツアキ and イケダ, マサヒロ and イトウ, カツアキ}
}