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  1. 30 医学部・医学研究科・保健学研究科
  2. 30b 弘前医学 = Hirosaki Medical Journal
  3. 61巻Supplement

<Syposium II>Inactivation of voltage-gated Ca^2+ channels and cone-rod dystrophy CORD7

http://hdl.handle.net/10129/3670
http://hdl.handle.net/10129/3670
a3795fde-b382-4710-ad48-9819083d0b75
名前 / ファイル ライセンス アクション
HirosakiMedJ_61_S53.pdf HirosakiMedJ_61_S53.pdf (288.0 kB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2010-08-16
タイトル
タイトル <Syposium II>Inactivation of voltage-gated Ca^2+ channels and cone-rod dystrophy CORD7
言語
言語 eng
キーワード
主題Scheme Other
主題 Calcium channel
キーワード
主題Scheme Other
主題 inactivation
キーワード
主題Scheme Other
主題 neurotransmission
キーワード
主題Scheme Other
主題 RIM
キーワード
主題Scheme Other
主題 Calcium channel; inactivCone-Rod Dystrophy
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
著者 Wakamori, Minoru

× Wakamori, Minoru

Wakamori, Minoru

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Uriu, Yoshitsugu

× Uriu, Yoshitsugu

Uriu, Yoshitsugu

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Miki, Takafumi

× Miki, Takafumi

Miki, Takafumi

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Kiyonaka, Shigeki

× Kiyonaka, Shigeki

Kiyonaka, Shigeki

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Mori, Yasuo

× Mori, Yasuo

Mori, Yasuo

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著者所属
値 Department of Oral Biology, Tohoku University Graduate School of Dentistry
著者所属
値 Department of Synthetic Chemistry and Biological Chemistry, Kyoto University Graduate School of Engineering
著者所属
値 Department of Synthetic Chemistry and Biological Chemistry, Kyoto University Graduate School of Engineering
著者所属
値 Department of Synthetic Chemistry and Biological Chemistry, Kyoto University Graduate School of Engineering
著者所属
値 Department of Synthetic Chemistry and Biological Chemistry, Kyoto University Graduate School of Engineering
抄録
内容記述タイプ Abstract
内容記述 Active zones are highly specialized sites for release of neurotransmitter in presynaptic nerve terminals. The spacing between voltage-dependent calcium channels( VDCCs) and synaptic vesicles at active zones is thought to infl uence the dynamic properties of synaptic transmission. Recently we have demonstrated a novel molecular interaction between VDCCs and an active zone scaffolding protein, rab3-interacting molecule 1 (RIM1). The RIM1 induced a pronounced deceleration of inactivation rate and a depolarizing shift of the inactivation curve of recombinant P/Q-type VDCC expressed as α1Aα2/δβ1a complex in baby hamster kidney cells. During 2-s voltagedisplacement to -30 mV, which is the threshold of the P/Q-type VDCC activation, almost all channels were inactivated in the absence of the RIM1 (closed-state inactivation), but less than 20% of the channels were inactivated in the presence of the RIM1. Thus, the RIM1 coordinates calcium signaling and spatial organization of molecular constituents at presynaptic active zone.
A mutation has been identified for an autosomal dominant cone-rod dystrophy CORD7 in the RIM1 gene. Interestingly, the aff ected individuals showed signifi cantly enhanced cognitive abilities across a range of domains. The mouse RIM1 arginine-to-histidine substitution (R655H), which corresponds to the human CORD7 mutation, modifi es RIM1 function in regulating VDCC currents elicited by the P/Q-type Cav2.1 and L-type Cav1.4 channels. The data can raise an interesting possibility that CORD7 phenotypes including retinal defi cits and enhanced cognition are at least partly due to altered regulation of presynaptic VDCC currents.
引用
内容記述タイプ Other
内容記述 弘前医学. 61(Suppl.), 2010, p.S53-S62
書誌情報 弘前医学

巻 61, 号 Supplement, p. S53-S62, 発行日 2010-07-08
ISSN
収録物識別子タイプ ISSN
収録物識別子 0439-1721
書誌レコードID
収録物識別子タイプ NCID
収録物識別子 AN00211444
著者版フラグ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
日本十進分類法
主題Scheme NDC
主題 490
NIIサブジェクト
主題Scheme Other
主題 医学
出版者
出版者 弘前大学大学院医学研究科・弘前医学会
資源タイプ
値 Article
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