Ahern G P, Junankar P R, Dulhunty A F
Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra City.
FEBS Lett. 1994 Oct 3;352(3):369-74. doi: 10.1016/0014-5793(94)01001-3.
The immunosuppressant drug FK-506 (3-20 microM) increased the open probability of ryanodine receptor calcium release channels, formed by incorporation of terminal cisternae vesicles from rabbit skeletal muscle into lipid bilayers, with cis (cytoplasmic) calcium concentrations between 10(-7) M and 10(-3) M. FK-506 increased mean current and channel open time and induced long sojourns at subconductance levels that were between 28% and 38% of the maximum conductance and were distinct from the ryanodine-induced subconductance level at about 45% of the maximum conductance. FK-506 relieved the Ca2+ inactivation of the ryanodine receptor seen at 10(-3) M Ca2+. The results are consistent with FK-506 removal of FK-506 binding protein from the ryanodine receptor.
免疫抑制剂FK - 506（3 - 20微摩尔）增加了雷诺丁受体钙释放通道的开放概率，该通道通过将兔骨骼肌终末池囊泡整合到脂质双层中形成，胞质侧（顺式）钙浓度在10⁻⁷摩尔/升和10⁻³摩尔/升之间。FK - 506增加了平均电流和通道开放时间，并在亚电导水平诱导了长时间停留，这些亚电导水平为最大电导的28%至38%，且与雷诺丁诱导的约为最大电导45%的亚电导水平不同。FK - 506缓解了在10⁻³摩尔/升钙离子浓度下观察到的雷诺丁受体的钙离子失活。这些结果与FK - 506从雷诺丁受体上移除FK - 506结合蛋白一致。
