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Mechanisms of interaction between the volume-sensitive outwardly rectifying anion channel, VSOR, and a novel membrane protein, LRRC8A.

Mechanisms of interaction between the volume-sensitive outwardly rectifying anion channel, VSOR, and a novel membrane protein, LRRC8A.
体积敏感的外向整流阴离子通道 VSOR 和新型膜蛋白 LRRC8A 之间的相互作用机制。
批准号:
15K15028
负责人:
OKADA Yasunobu
金额:
$2.41万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Challenging Exploratory Research
财政年份:
2015
资助国家:
日本
项目状态:
已结题
起止时间:
2015-04-01 至 2017-03-31

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中文摘要
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期刊论文(8)
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会议论文
LRRC8 family is involved in volume-sensitive outwardly rectifying anion channel (VSOR) activity but not in acid-sensitive outwardly rectifying anion channel (ASOR) activity.
LRRC8 家族参与体积敏感的外向整流阴离子通道 (VSOR) 活性,但不参与酸敏感的外向整流阴离子通道 (ASOR) 活性。
DOI: --
发表时间: 2017
期刊:
影响因子: --
作者: [Sato-Numata K, Numata T, Inoue R, Sabirov RZ, Okada Y]
通讯作者: Okada Y
Pharmacological distinction between acid-sensitive outwardly rectifying anion channel (ASOR) and volume-sensitive outwardly rectifying anion channel (VSOR).
酸敏感型外向整流阴离子通道(ASOR)和体积敏感型外向整流阴离子通道(VSOR)之间的药理学区别。
DOI: --
发表时间: 2016
期刊:
影响因子: --
作者: [Sato-Numata K, Numata T, Inoue R, Okada Y]
通讯作者: Okada Y
Channeling frozen cells to survival after thawing: opening the door to cryo-physiology.
引导冷冻细胞解冻后存活:打开冷冻生理学之门。
DOI: 10.1113/jp271842
发表时间: 2016
期刊: J. Physiol. (London)
影响因子: --
作者: [Matsumoto M, Hiyama TY, Kuboyama K, Suzuki R, Fujikawa A, Noda M., Y. Okada]
通讯作者: Y. Okada
シスプラチン耐性細胞株KCP-4におけるLRRC8分子群の役割の検討
LRRC8分子在顺铂耐药细胞系KCP-4中的作用研究
DOI: --
发表时间: 2016
期刊:
影响因子: --
作者: [岡田俊昭, Md.R. Islam, N.A. Tsiferova, R.S. Kurbannazarova, 岡田泰伸, R.Z. Sabirov]
通讯作者: R.Z. Sabirov
Elucidation of hypotonicity-induced suppression mechanism of vasopressin secretion through identification of hypoosmolarity sensor
  • 批准号:
    23659118
  • 项目类别:
    Grant-in-Aid for Challenging Exploratory Research
  • 资助金额:
    $2.41万
  • 财政年份:
    2011
  • 负责人:
    OKADA Yasunobu
  • 依托单位:
Molecular characterization of volume-activated anion channels and elucidation of cell death-survival switching mechanisms
Channel-mediated mechanisms of induction of and protection against cell death
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