CALCIUM AS A COAGONIST OF INOSITOL 1,4,5-TRISPHOSPHATE INDUCED CALCIUM RELEASE
CALCIUM AS A COAGONIST OF INOSITOL 1,4,5-TRISPHOSPHATE INDUCED CALCIUM RELEASE
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DOI：
10.1126/science.2017683
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发表时间：
1991-04-19
期刊：
影响因子：
56.9
通讯作者：
GOLDIN, SM
中科院分区：
文献类型：
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作者：
FINCH, EA;TURNER, TJ;GOLDIN, SM
肌醇1，4，5-三磷酸（IP 3）诱导的细胞内钙释放是细胞内游离钙水平的调节剂。亚秒级动力学和调节IP 3诱导的钙-45释放突触体衍生的微粒体囊泡解决了快速灌流。囊外钙作为凝血剂，增强瞬时IP 3诱导的钙-45释放。因此，胞质钙水平的快速升高可能触发体内IP 3诱导的钙释放。囊外钙还对IP 3诱导的钙-45释放产生了更缓慢的、可逆的抑制作用。钙离子对IP 3诱导的钙离子释放的顺序正反馈和负反馈调节可能有助于体内胞质游离钙离子的瞬变和振荡。
Inositol 1,4,5-trisphosphate (IP3)-induced calcium release from intracellular stores is a regulator of cytosolic-free calcium levels. The subsecond kinetics and regulation of IP3-induced calcium-45 release from synaptosome-derived microsomal vesicles were resolved by rapid superfusion. Extravesicular calcium acted as a coagonist, potentiating the transient IP3-induced release of calcium-45. Thus, rapid elevation of cytosolic calcium levels may trigger IP3-induced calcium release in vivo. Extravesicular calcium also produced a more slowly developing, reversible inhibition of IP3-induced calcium-45 release. Sequential positive and negative feedback regulation by calcium of IP3-induced calcium release may contribute to transients and oscillations of cytosolic-free calcium in vivo.