Study of TRIC and MG23 channels

TRIC和MG23通道的研究

• 批准号: 23240055
• 负责人: TAKESHIMA Hiroshi
• 金额: $ 31.62万
• 依托单位: Kyoto University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (A)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011-04-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-23240055/
• 关键词: TRICチャネル; 小胞体Ca2+放出; 血管平滑筋; ミツグミン２３; Ca2+スパーク; ミツグミン53; TRIM50; ミツグミン23; 脂質二重膜再構成; 単粒子解析; リアノジン受容体; 高血圧

TRIC-A-knockout mice develop hypertension due to elevated myogenic tonus in resistance artery. By analyzing TRIC-A-knockout and overexpression mice, we found that TRIC-A density restricts Ca2+ spark frequency in vascular smooth muscle.Mitsugumin 23 is an unknown membrane protein in the endo/sarcoplasmic reticulum. Our studies revealed that mitsugumin 23 forms an homo-maltimer with a bowl-like stereostructure and exhibits unstable cation channel activity.

trica - a基因敲除小鼠因阻力动脉肌张力升高而发生高血压。通过分析trica - a敲除和过表达小鼠，我们发现trica - a密度限制血管平滑肌Ca2+火花频率。mitsugumin23是一种未知的内/肌浆网膜蛋白。我们的研究表明，mitsugumin23形成具有碗状立体结构的同源maltimer，并表现出不稳定的阳离子通道活性。

项目成果

TRIC channels are essential partners for Ca^<2+> release

TRIC 通道是 Ca^<2> 释放的重要合作伙伴

• 发表时间: 2012
• 作者: Takeshima;H
• 通讯作者: H

TRIC channels supporting physiological Ca^<2+> release

TRIC 通道支持生理 Ca^<2 > 释放

• 发表时间: 2012
• 作者: Takeshima;H
• 通讯作者: H

Sarcalumenin plays a critical role in age-related cardiac dysfunction due to decreases in SERCA2a expression and activity

• DOI: 10.1016/j.ceca.2011.10.003
• 发表时间: 2012-01-01
• 期刊: CELL CALCIUM
• 影响因子: 4
• 作者: Jiao, Qibin;Takeshima, Hiroshi;Minamisawa, Susumu
• 通讯作者: Minamisawa, Susumu

TRIC channel subtypes, willing partners with Ca2+ release channels in intracellular stores

TRIC 通道亚型，愿意与细胞内存储中的 Ca2 释放通道合作

• 发表时间: 2011
• 作者: Takeshima;H.
• 通讯作者: H.

TRIC channels and vascular tonus

TRIC 通道和血管紧张度

• 作者: Takeshima;H.
• 通讯作者: H.