The actin cytoskeleton diffeirentially regulates NG115-401L cell ryanodine receptor and inositol 1,4,5-trisphosphate receptor induced calcium signaling pathways

被引：10

作者：

Bose, Diptiman D. ^{[2
]}

Thomas, David W. ^{[1
]}

机构：

[1] Univ Pacific, Thomas J Long Sch Pharm & Hlth Sci, Dept Physiol & Pharmacol, Stockton, CA 95211 USA

[2] Univ Calif Davis, Sch Vet Med, Dept Mol Biosci, Davis, CA 95616 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2009年 / 379卷 / 02期

关键词：

Ca2+; Actin; Cytoskeleton; Inositol 1,45-trisphosphate receptor; Ryanodine receptor; Ca2+ release; Ca2+ influx; ENTRY; CHANNELS; ACTIVATION; VERSATILITY; MECHANISM; LINE;

D O I：

10.1016/j.bbrc.2008.12.138

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Regulation of bi-directional communication between intracellular Ca2+ pools and surface Ca2+ channels remains incompletely characterized. We report Ca2+ release mediated by inositol 1,4,5-trisphosphate receptor (IP3R) and ryanodine receptor (RyR) pathways is diminished under actin cytoskeleton disruption in NG 115-401L (401 L) neuronal cells, yet despite truncated Ca2+ release, Call influx was not significantly altered in these experiments. However, disruption of cortical actin networks completely abolished IP3R induced Ca2+ release, whereas RyR-mediated Ca2+ release was preserved, albeit attenuated. Moreover, cortical actin disruption completely abolished IP3R and RyR linked Ca2+ influx even though Ca2+ pool sensitivities were different. These findings suggest discrete Ca2+ store/Ca2+ channel coupling mechanisms in the IP3R and RyR pathways as revealed by the differential sensitivity to actin perturbation. (C) 2008 Elsevier Inc. All rights reserved.

引用

页码：594 / 599

页数：6

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