Removal of FKBP12.6 does not alter the conductance and activation of the cardiac ryanodine receptor or the susceptibility to stress-induced ventricular arrhythmias.

@article{Xiao2007RemovalOF,
  title={Removal of FKBP12.6 does not alter the conductance and activation of the cardiac ryanodine receptor or the susceptibility to stress-induced ventricular arrhythmias.},
  author={Jianmin Xiao and Xixi Tian and Peter P Jones and J. H. Bolstad and Huihui Kong and Ruiwu Wang and Lin Zhang and Henry J. Duff and Anne Gillis and Sidney Fleischer and Michael Kotlikoff and Julio A. Copello and S R Wayne Chen},
  journal={The Journal of biological chemistry},
  year={2007},
  volume={282 48},
  pages={34828-38}
}
The 12.6-kDa FK506-binding protein (FKBP12.6) is considered to be a key regulator of the cardiac ryanodine receptor (RyR2), but its precise role in RyR2 function is complex and controversial. In the present study we investigated the impact of FKBP12.6 removal on the properties of the RyR2 channel and the propensity for spontaneous Ca(2+) release and the occurrence of ventricular arrhythmias. Single channel recordings in lipid bilayers showed that FK506 treatment of recombinant RyR2 co-expressed… CONTINUE READING

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