WEKO3
アイテム
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The platelets were defective in aggregation and release reaction in response to synthetic TXA_2 mimetic (STA_2). When the platelet TXA_2 receptor was examined with both a [^\u003c125\u003eI]-labeled derivative of a TXA_2 receptor antagonist ([^\u003c125\u003eI]-PTAOH) and [^3H]-labeled TXA_2 agonist ([^3H]U-46619), the equilibrium dissociation rate constants(Kd)and the maximal concentrations of binding sites (Bmax) of the platelets to both ligands were within normal ranges, suggesting that the binding capacity of their TXA_2 receptor was normal. STA_2 could not induce IP3 formation and intracellular Ca^\u003c2+\u003e mobilization, whereas these responses to thrombin were within normal ranges. GTP ase activity was also decreased when the patient\u0027s platelet membrane was challenged with STA_2. Furthermore, we identified a single amino acid substitution (Arg^\u003c60\u003e→Leu) in the first cytoplasmic loop of the patient\u0027s platelet TXA_2 receptor. The mutant receptor expressed in Chinese hamster ovary cells showed decreased TXA_2-induced second messenger formation despite its normal ligand binding affinities. 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トロンボキサンA_2による血小板活性化機構 : トロンボキサン不応症における解析から
http://hdl.handle.net/10191/45512
http://hdl.handle.net/10191/45512b81a06b6-d504-4d59-b3d7-c4c48e3cd205
名前 / ファイル | ライセンス | アクション |
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111(11)_676-682.pdf (1.1 MB)
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Item type | 紀要論文 / Departmental Bulletin Paper(1) | |||||
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公開日 | 2017-01-13 | |||||
タイトル | ||||||
タイトル | トロンボキサンA_2による血小板活性化機構 : トロンボキサン不応症における解析から | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | トロンボキサンA_2による血小板活性化機構 : トロンボキサン不応症における解析から | |||||
言語 | ||||||
言語 | jpn | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | platelets | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | thromboxane A_2(TXA_2) receptor | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | defective TXA_2-induced platelet aggregation | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | G protein | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | phospholipase C | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | point mutation | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | 血小板 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | トロンボキサンA_2受容体 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | トロンボキサン不応症 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | G蛋白 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | 遺伝子解析 | |||||
資源タイプ | ||||||
資源 | http://purl.org/coar/resource_type/c_6501 | |||||
タイプ | departmental bulletin paper | |||||
その他のタイトル | ||||||
その他のタイトル | Pathogenetic Analysis of a Platelet Disorder Characterized by the Absence of Thromboxane A_2-Induced Platelet Aggregation | |||||
著者 |
布施, 一郎
× 布施, 一郎 |
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著者別名 | ||||||
識別子 | 107341 | |||||
識別子Scheme | WEKO | |||||
姓名 | Fuse, Ichiro | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | A patient with a mild bleeding disorder whose platelets responded defectively to thromboxane A_2 (TXA_2) was identified, and the mechanism of this dysfunction was analyzed. The platelets were defective in aggregation and release reaction in response to synthetic TXA_2 mimetic (STA_2). When the platelet TXA_2 receptor was examined with both a [^<125>I]-labeled derivative of a TXA_2 receptor antagonist ([^<125>I]-PTAOH) and [^3H]-labeled TXA_2 agonist ([^3H]U-46619), the equilibrium dissociation rate constants(Kd)and the maximal concentrations of binding sites (Bmax) of the platelets to both ligands were within normal ranges, suggesting that the binding capacity of their TXA_2 receptor was normal. STA_2 could not induce IP3 formation and intracellular Ca^<2+> mobilization, whereas these responses to thrombin were within normal ranges. GTP ase activity was also decreased when the patient's platelet membrane was challenged with STA_2. Furthermore, we identified a single amino acid substitution (Arg^<60>→Leu) in the first cytoplasmic loop of the patient's platelet TXA_2 receptor. The mutant receptor expressed in Chinese hamster ovary cells showed decreased TXA_2-induced second messenger formation despite its normal ligand binding affinities. These results suggest that the Arg^<60> to Leu mutation is responsible for the disorder and that this region could also comprise an important functional element for interaction with G protein linked to PLC. | |||||
書誌情報 |
新潟医学会雑誌 en : 新潟医学会雑誌 巻 111, 号 11, p. 676-682, 発行日 1997-11 |
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出版者 | ||||||
出版者 | 新潟医学会 | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 00290440 | |||||
書誌レコードID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AN00182415 | |||||
著者版フラグ | ||||||
値 | publisher |