Calcium modulation of inositol 1,4,5-trisphosphate-induced calcium release from neuroblastoma x glioma hybrid (NG108-15) microsomes.
Calcium modulation of inositol 1,4,5-trisphosphate-induced calcium release from neuroblastoma x glioma hybrid (NG108-15) microsomes.
复制标题
肌醇 1,4,5-三磷酸诱导的神经母细胞瘤 x 神经胶质瘤杂交体 (NG108-15) 微粒体钙释放的钙调节。
DOI：
10.1016/s0021-9258(18)66582-2
复制
发表时间：
1986
期刊：
影响因子：
--
通讯作者：
C. Klee
中科院分区：
文献类型：
--
作者：
T. Jean;C. Klee
采用神经母细胞瘤-神经胶质瘤(NG108-15)杂交细胞亚细胞组分，研究了1，4，5-三磷酸肌醇诱导细胞内钙释放的机制。微体部分富含内质网和质膜，几乎没有线粒体，是依赖三磷酸肌醇或GTP释放钙的最活跃的部分。GTP和1，4，5-三磷酸肌醇均不影响另一种试剂介导的钙外流，提示三磷酸肌醇和三磷酸肌醇作用于不同的钙滞留囊泡。GTP对钙释放的刺激作用相对较慢(t1/2=90 S)，且呈聚乙二醇依赖性，2×10(-5)M钙(5nmoXmin-1×mg-1)的刺激作用大于10(-6)M钙(0.8nmoXmin-1×mg-1)。肌醇一磷酸不能模拟肌醇引起的钙外流，这种作用迅速(t_(1/2)小于10 S)，不受3%聚乙二醇的影响。三磷酸肌醇在10(-6)M外加钙(1nmoXmin-1×mg-1)时释放量最大，在2×10(-5)M钙时无法检测到。胞浆钙反馈抑制三磷酸肌醇诱导的钙释放，提供了一种防止异常高钙的有害影响的安全机制。
Subcellular fractions of neuroblastoma x glioma (NG108-15) hybrid cells were used to study the mechanism of inositol 1,4,5-trisphosphate-induced calcium release. A microsomal fraction, enriched in endoplasmic reticulum and plasma membranes and almost devoid of mitochondria, was the most active in inositol trisphosphate- or GTP-dependent release of calcium. Neither GTP nor inositol 1,4,5-trisphosphate affected the calcium efflux mediated by the other reagent, suggesting that inositol trisphosphate and GTP act on different calcium-sequestrating vesicles. The stimulation of calcium release by GTP was relatively slow (t1/2 = 90 s), dependent on polyethyleneglycol, and greater at 2 X 10(-5) M calcium (5 nmol X min-1 X mg-1) than at 10(-6) M calcium (0.8 nmol X min-1 X mg-1). The inositol trisphosphate-induced calcium efflux was not mimicked by inositol monophosphate; it was fast (t1/2 less than 10 s) and unaffected by 3% polyethyleneglycol. The amount of calcium released by inositol trisphosphate was greatest at 10(-6) M external calcium (1 nmol X min-1 X mg-1) and it was undetectable at 2 X 10(-5) M calcium. A feedback inhibition of the inositol trisphosphate-induced calcium release by cytoplasmic calcium provides a safety mechanism preventing deleterious effects of abnormally high calcium levels.