Absence of a Trafficking Defect in R1232W/T1620M, a Double SCN5A Mutant Responsible for Brugada Syndrome
スポンサーリンク
概要
- 論文の詳細を見る
Background A trafficking defect of mutant cardiac Na-channels (SCN5A) has been implicated in Brugada syndrome. Although R1232W polymorphism and T1620M mutation by themselves have little effect on Na-channel function, their combination has been reported to disrupt membrane trafficking, resulting in a non-functioning Na channel. Methods and Results Contrary to previous findings, patch-clamp recordings of heterologously expressed R1232W/T1620M showed robust Na currents and confocal microscopy exhibited predominant expression in the plasma membrane, similar to the wild-type channel. Conclusions It is unlikely that an intragenic interaction between R1232W and T1620M of SCN5A causes a trafficking defect leading to a non-functioning Na channel.
- 社団法人日本循環器学会の論文
- 2008-05-20
著者
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Tsutsui Hiroyuki
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Hokkaido University
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MAKITA Naomasa
Department of Cardiovascular Medicine, Hokkaido University Graduate School of Medicine
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Mochizuki Naoki
Department of Cardiology, National Cardiovascular Center
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Makita Naomasa
Department Of Cardiovascular Medicine Hokkaido University Graduate School Of Medicine
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Mochizuki Naoki
Department Of Structural Analysis National Cardiovascular Center Research Institute
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Makita Naomasa
Department Of Gastroenterology National Hospital Organization Kyushu Medical Center
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Tsutsui Hiroyuki
Department Of Cardiovascular Medicine
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Makita Naomasa
Department Of Cardiovascular Medichine Hokkaido University School Of Medicine
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Makita Naomasa
Department Of Cadiovascular Medicine Hokkaido University Graduate School Fo Medicine
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