Brillantes A B, Ondrias K, Scott A, Kobrinsky E, Ondriasová E, Moschella M C, Jayaraman T, Landers M, Ehrlich B E, Marks A R
Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029.
Cell. 1994 May 20;77(4):513-23. doi: 10.1016/0092-8674(94)90214-3.
FK506-binding protein (FKBP12) was originally identified as the cytosolic receptor for the immunosuppressant drugs FK506 and rapamycin. The cellular function of FKBP12, a ubiquitously expressed 12,000-dalton proline isomerase, has been unknown. FKBP12 copurifies with the 565,000-dalton ryanodine receptor (RyR), four of which form intracellular Ca2+ release channels of the sarcoplasmic and endoplasmic reticula. By coexpressing the RyR and FKBP12 in insect cells, we have demonstrated that FKBP12 modulates channel gating by increasing channels with full conductance levels (by > 400%), decreasing open probability after caffeine activation (from 0.63 +/- 0.09 to 0.04 +/- 0.02), and increasing mean open time (from 4.4 +/- 0.6 ms to 75 +/- 41 ms). FK506 or rapamycin, inhibitors of FKBP12 isomerase activity, reverse these stabilizing effects. These results provide the first natural cellular function for FKBP12, and establish that the functional Ca2+ release channel complex includes FKBP12.
FK506结合蛋白(FKBP12)最初被鉴定为免疫抑制剂FK506和雷帕霉素的胞质受体。FKBP12是一种普遍表达的12000道尔顿的脯氨酸异构酶,其细胞功能一直未知。FKBP12与565000道尔顿的兰尼碱受体(RyR)共纯化,其中四个形成肌浆网和内质网的细胞内Ca2+释放通道。通过在昆虫细胞中共表达RyR和FKBP12,我们证明FKBP12通过增加具有全电导水平的通道(增加>400%)、降低咖啡因激活后的开放概率(从0.63±0.09降至0.04±0.02)以及增加平均开放时间(从4.4±0.6毫秒增至75±41毫秒)来调节通道门控。FKBP12异构酶活性的抑制剂FK506或雷帕霉素可逆转这些稳定作用。这些结果首次揭示了FKBP12的天然细胞功能,并证实功能性Ca2+释放通道复合物包含FKBP12。