22 Papers
374 Citations
Bin Ye is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Long QT syndrome & Sudden death. The author has an hindex of 19, co-authored 21 publications.
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Papers
Properties of HERG channels stably expressed in HEK 293 cells studied at physiological temperature.
Zhengfeng Zhou,Qiuming Gong,Bin Ye,Zheng Fan,Jonathan C. Makielski,Gail A. Robertson,Craig T. January +6 more
TL;DR: The data support the postulate that HERG encodes a major constituent of I(Kr) and suggest that at physiological temperatures HERG contributes current throughout most of the action potential and into the postrepolarization period.
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Novel mechanism for sudden infant death syndrome: Persistent late sodium current secondary to mutations in caveolin-3
Lisa B. Cronk,Bin Ye,Toshihiko Kaku,David J. Tester,Matteo Vatta,Matteo Vatta,Jonathan C. Makielski,Michael J. Ackerman +7 more
TL;DR: This study provides the first molecular and functional evidence implicating CAV3 as a pathogenic basis of SIDS and shows that the LQT3-like phenotype of increased late sodium current supports an arrhythmogenic mechanism for some cases of Sids.
271
A common human SCN5A polymorphism modifies expression of an arrhythmia causing mutation
TL;DR: The results show that the choice of background clone must be carefully considered in mutagenesis studies, as SCN5A encodes the alpha-subunit of the ion channel that carries Na current in human heart.
175
Common human SCN5A polymorphisms have altered electrophysiology when expressed in Q1077 splice variants
Bi-Hua Tan,Carmen R. Valdivia,Benjamin A. Rok,Bin Ye,Karen M. Ruwaldt,David J. Tester,Michael J. Ackerman,Jonathan C. Makielski +7 more
TL;DR: The majority of common human SCN5A polymorphisms have a distinct molecular phenotype that depends upon the splice variant background, and these findings have implications for the interpretation of previous studies of arrhythmia mutations.
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A novel SCN5A arrhythmia mutation, M1766L, with expression defect rescued by mexiletine
Carmen R. Valdivia,Michael J. Ackerman,David J. Tester,Tomoyuki Wada,Jorge McCormack,Bin Ye,Jonathan C. Makielski +6 more
TL;DR: Findings suggest that M1766L-SCN5A channel dysfunction may contribute to the basis of lethal arrhythmias, displays an overlapping electrophysiological phenotype, and represents the first sodium channelopathy rescued by drug.
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