Mechanisms of receptor-operated Ca^<2+> entry-Molecular structures and the function of store-operated Ca^<2+>entry and its blockers.
Mechanisms of receptor-operated Ca^<2+> entry-Molecular structures and the function of store-operated Ca^<2+>entry and its blockers.
批准号:
11470392
负责人:
DOHI Toshihiro
金额:
$9.28万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B).
财政年份:
1999
资助国家:
日本
项目状态:
已结题
起止时间:
1999 至 2000
中文摘要
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英文摘要
The receptor-activated Ca^<2+> channels (ROC) activate Ca^<2+> entry which is activated by the depletion of intracellular Ca^<2+> stores, termed store-operated channels (SOC). However, the structure and function of these channels are still unidentified, and the specific blockers are not developed. The present study was undertaken to elucidate the mechanisms for the activation of and the signal transduction relate to ROC/SOC, and inhibitors for the channels.1 COS cells were expressed with rat TRP by introducing rtrp3 and rtrp6. These COS cells were treated with thapsigargin in the absence of extracellular Ca^<2+> to acivate SOC.Large Ca^<2+> entry was observed in these cells. PC12 cells expressed dominantly trp1 and trp3. In PC12 cells introduced trp1,3 antisense mRNA, Ca^<2+> entry evoked by the pre-treatment of acetylcholine and thapsigargine was enhanced. These results may suggest that TRPs do not simply compose the Ca^<2+> channel itself but relate somehow with SOC systems.2 12-hydr … More oxyeicosatetraenoic acid (12-HETE), a mediator of inflammation. activates neutrophils through the rise of intracellular free Ca^<2+> concentration ([Ca^<2+>]i). However, the mechanism of Ca^<2+> rise was not evident. 12-HETE-induced [Ca^<2+>]i rise was blocked by platelet-activating factor(PAF) antagonist, PAF synthesis inhibitor and 12-HETE stimulated PAF production in human and rabbit neutophils. These results suggested that 12-HETE-induced [Ca^<2+>]i rise is mediated by PAF.FMLP-but not LTB_4-induced [Ca^<2+>]i rise was partly mediated by PAF.3 Pituitary adenylate cyclase activating polypeptide (PACAP) induced long-lasting increase in [Ca^<2+>]i and catecholamine release from bovine adrenal chromaffin cells. PACAP-induced ([Ca^<2+>]i rise was not mediated by cyclic AMP, phospholipase C, cyclic ADP-ribose, voltage-dependent Na+ channels, voltage-dependent Ca^<2+> channels. Pre-activation of SOC did not modify PACAP-induced Ca^<2+> entry. GdCl_2 blocked SOC but did not affect PACAP-induced Ca^<2+> entry. These results suggested that PACAP activates ROC which is distinguishable form SOC.4 Caffeine and theophylline were found to block [Ca^<2+>]i rise and Ca^<2+> entry induced by acetylcholine, thapsigargine and TPEN in bovine adrenal chromaffin cells. Less
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K.Shibata,H.Yoshino,N.Mizuno,H.Shinohara,K.Morita,S.Kitayama,H.Kurihara,T.Dohi: "Mediation by platelet-activating factor of 12-hydroxyeicosatetraenoic acid-induced cytosolic free calcium concentration elevation in neutorphils."Prostaglandins & other Lipid
K.Shibata,H.Yoshino,N.Mizuno,H.Shinohara,K.Morita,S.Kitayama,H.Kurihara,T.Dohi:“血小板活化因子对 12-羟基二十碳四烯酸诱导的胞质游离钙浓度的调节
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森田克也: "Ca^<2+>動員物質サイクリックADPリボースの合成酵素および細胞膜輸送体としてのCD38"ファルマシア. 35. 946-947 (1999)
Katsuya Morita:“CD38作为Ca 2+ 动员物质环ADP核糖的合酶和细胞膜转运蛋白”Pharmacia 35. 946-947 (1999)。
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森田克也: "Ca^<2+>動員物質サイクリックADPリボースの合成および細胞膜輸送体としてのCD38"ファルマシア. 35. 946-947 (1999)
Katsuya Morita:“Ca 2+ 动员物质环ADP核糖和CD38作为细胞膜转运蛋白的合成”Pharmacia 35. 946-947 (1999)。
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Shibata, K., Yoshino, H., Mizuno, N., Shinohara, H., Morita, K., Kitayama, S., Kurihara, H.and Dohi, T.: "Mediation of platelet-activating factor of 12-hydroxyeicosatetraenoic acid-induced cytosolic free calcium concentration elevation in neutrophils."Pro
Shibata, K.、Yoshino, H.、Mizuno, N.、Shinohara, H.、Morita, K.、Kitayama, S.、Kurihara, H. 和 Dohi, T.:“12-血小板活化因子的介导
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Morita, K.: "CD38 as an enzyme for the synthesis of cyclic ADP-ribose, an endogenous Ca^<2+> mobilizing substance and for the transmembrane carrier of the nucleotide."Farumashia. 35. 946-947 (1999)
Morita, K.:“CD38作为一种酶,用于合成环状ADP-核糖、一种内源性Ca 2+ 动员物质以及核苷酸的跨膜载体。”Farumashia。
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