Molecular Medicine FKBP12 Is a Critical Regulator of the Heart Rhythm and the Cardiac Voltage-Gated Sodium Current in Mice

نویسندگان

  • Mitsunori Maruyama
  • Bai-Yan Li
  • Hanying Chen
  • Xuehong Xu
  • Long-Sheng Song
  • Silvia Guatimosim
  • Wuqiang Zhu
  • Weidong Yong
  • Wenjun Zhang
  • Guixue Bu
  • Shien-Fong Lin
  • Michael C. Fishbein
  • W. Jonathan Lederer
  • John H. Schild
  • Loren J. Field
  • Michael Rubart
  • Peng-Sheng Chen
  • Weinian Shou
چکیده

voltage-gated sodium current INa in MyHC-FKBP12 ventricular cardiomyocytes, a slower recovery of INa from inactivation, shifts of steady-state activation and inactivation curves of INa to more depolarized potentials, and augmentation of late INa, suggesting that the arrhythmogenic phenotype of MyHC-FKBP12 mice is attributable to abnormal INa. Ventricular cardiomyocytes isolated from FKBP12 / MyHC-Cre hearts showed faster action potential upstrokes and a more than 2-fold increase in peak INa density. Dialysis of exogenous recombinant FKBP12 protein into FKBP12-deficient cardiomyocytes promptly recapitulated

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FKBP12 is a critical regulator of the heart rhythm and the cardiac voltage-gated sodium current in mice.

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تاریخ انتشار 2011