Role of transmembrane protein 168 mutations in Brugada syndrome by alteration in subcellular localization of αB-crystallin to modulate sodium channel Na <SUB>v</SUB>1.5 surface expression in cardiomyocytes

Nguyen Le Kim Chi

[1P-091（2T07a-08）] Role of transmembrane protein 168 mutations in Brugada syndrome by alteration in subcellular localization of αB-crystallin to modulate sodium channel Na _v1.5 surface expression in cardiomyocytes

^〇Nguyen Le Kim Chi¹, Akio Shimizu¹, Akira Sato¹, Hisakazu Ogita¹ (Division of Molecular Medical Biochemistry, Department of Biochemistry and Molecular Biology, Shiga University of Medical Science)

キーテクノロジー：immunostainning,western blot

Transmembrane protein 168、Brugada syndrome、α B-crystallin、cardiac sodium channel

bschikim@gmail.com

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The 95th Annual Meeting of the Japanese Biochemical Society

[1P-091（2T07a-08）] Role of transmembrane protein 168 mutations in Brugada syndrome by alteration in subcellular localization of αB-crystallin to modulate sodium channel Na _v1.5 surface expression in cardiomyocytes

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The 95th Annual Meeting of the Japanese Biochemical Society

[1P-091（2T07a-08）] Role of transmembrane protein 168 mutations in Brugada syndrome by alteration in subcellular localization of αB-crystallin to modulate sodium channel Na v1.5 surface expression in cardiomyocytes

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[1P-091（2T07a-08）] Role of transmembrane protein 168 mutations in Brugada syndrome by alteration in subcellular localization of αB-crystallin to modulate sodium channel Na _v1.5 surface expression in cardiomyocytes