三磷酸肌醇影响钙释放的两个作用

The Research of Mathematical Model for Inositol-1,4,5-Trisphate-induced Ca^(2+) Oscillations

此模型主要说明激动剂诱发的 Ca2 +振荡实验中影响 Ca2 +释放的两个因素 :(a)三磷酸肌醇 (IP3)抑制Ca2 + 从内质网 ER中释放。 (b) IP3通过 Gq作用磷酸酶 C促使 Ca2 + 从 ER释放。模型假设 ER上 IP3受体是相互独立的亚基组成的四聚物 ,每个亚基可以结合 Ca2 + 和 IP3。IP3受体 / Ca2 + 通道的缓慢恢复到稳定状态是钙对自身释放抑制的原因。钙振荡的关键是最大 Ca2 +依赖性 IP3的进入速率 (v6 )和 IP3的衰减时间常数 (v7)的比值 : 当 v6 / v7<0 .2 8,不振荡 ;II当 0 .2 8<v6 / v7<0 .5 72振荡 ;III当 v6 / v7>0 .5

This article mainly illustrates the model for against-stimulated Ca2+ oscillations that involves two roles for cytosolic Ca2+ :(a) inositol-1.4.5-triphosphate(IP3) inhibits Ca2+ release from the endoplasmic reticulum (ER); (b) IP3 acts on phosphate C, via a Gq protein related mechanism and hence stimulates Ca2+ release from ER. The model assumes that the ER IP3 receptor is a tetramer of independent subunit that can bind both Ca2+ and IP3. The reason for inhibition of Ca2+ oscillations is that IP3-receptor/Ca2+ -channel slowly comes back to the beginning stable state. The key parameter for Ca2+ oscillations is the ratio of Maximum Ca2+ dependent IP3 input rate (v6) to IP3 decay rate constant(v7): I when v6/v7 less than or equal 0.28, no oscillation could be found; II when 0.28 less than or equal v6/v7 less than or equal 0.572, oscillation starts; III when v6/v7>0.572, Ca2+ ceases and arrives at a stable state quickly.