Taylor C W, Putney J W
Biochem J. 1985 Dec 1;232(2):435-8. doi: 10.1042/bj2320435.
Permeabilized hepatocytes accumulated 45Ca2+ into a non-mitochondrial pool when provided with ATP. 45Ca2+ efflux from this pool was revealed by removal of ATP with glucose and hexokinase or by inhibiting uptake with NaVO3. The effect of inositol 1,4,5-trisphosphate (IP3) on 45Ca2+ efflux from the pool was investigated. IP3 (5 microM) evoked a rapid increase in the rate of 45Ca2+ efflux. Kinetic analysis of the effect of IP3 indicated the existence of two distinct Ca2+ fractions within the pool; only one, accounting for about one-third of the ATP-dependent Ca2+ content of the pool, was responsive to IP3. The effect of IP3 on 45Ca2+ efflux from the non-mitochondrial pool does not require ATP, a finding that is inconsistent with a previous suggestion that this effect may be mediated by protein phosphorylation.
当提供ATP时,通透化的肝细胞将45Ca2+积累到一个非线粒体池中。通过用葡萄糖和己糖激酶去除ATP或用钒酸钠抑制摄取,可显示该池中45Ca2+的流出。研究了肌醇1,4,5-三磷酸(IP3)对该池中45Ca2+流出的影响。IP3(5微摩尔)引起45Ca2+流出速率迅速增加。对IP3作用的动力学分析表明,该池内存在两个不同的Ca2+组分;只有一个组分,约占该池ATP依赖性Ca2+含量的三分之一,对IP3有反应。IP3对非线粒体池中45Ca2+流出的作用不需要ATP,这一发现与先前认为该作用可能由蛋白质磷酸化介导的观点不一致。