日本生理学会大会発表要旨集
日本生理学会大会発表要旨集
セッションID: 1S01A2
会議情報
Regulation of ion channels and transporters through the protein–protein interactions
一酸化窒素によるイオンチャネル制御機構:カベオラ・ラフトにおける動的タンパク間相互作用の役割
古川 哲史白 長喜黒川 洵子
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会議録・要旨集 フリー

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Nitric oxide (NO) is a gaseous signaling molecule, having diverse biological actions. In addition to the well-known guanylate cyclase/cGMP/protein kinase G pathway, direct protein s-nitrosylation and s-glutathiolation provide a novel mechanism of NO-dependent signaling. In cardiac myocytes, the slowly activating delayed rectifier potassium current (IKs) channels appear to co-localize with NO synthase-3 (NOS3) in caveolae (ref 1), and is a target of s-nitrosylation by NO (ref 2). S-nitrosylation by NO underlies physiologically important regulatory mechanisms of IKs by cytosolic Ca2+ and by sex hormones. Rise in intracellular Ca2+ activates NOS3 and produces NO via a Ca2+/calmodulin-dependent pathway, resulting in activation of IKs channel (ref 3). Sex hormones, such as testosterone, estradiol, and progesterone, activate NOS3 via their non-genotropic pathway, which also enhances IKs (ref 4). It has been shown that scaffolding proteins belonging to striatin family (striatin, zinedin, and SG2NA) compose macromolecular complex involving caveolin, calmodulin, NOS, and sex hormone receptor. Dynamic changes in protein-protein interaction around this macromolecular complex play an important role in NO-dependent IKs regulation. [References] (1) J. Biol. Chem. 2004;279:40778-40787.(2) Br. J. Pharmacol. 2004;142:567-575.(3) Circ. Res. 2005;96:64-72.(4) Circulation (in revision). [Jpn J Physiol 55 Suppl:S6 (2005)]
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© 2005 日本生理学会
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