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首页> 外文期刊>American Journal of Physiology >Serum- and glucocorticoid-Inducible kinase SGK1 regulates reorganization of actin cytoskeleton in mast cells upon degranulation
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Serum- and glucocorticoid-Inducible kinase SGK1 regulates reorganization of actin cytoskeleton in mast cells upon degranulation

机译:血清和糖皮质激素诱导激酶SGK1调节肥大细胞脱粒后肌动蛋白细胞骨架的重组

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摘要

Aggregation of the high-affinity IgE receptor (FceRI) on mast cells (MCs) causes MC degranulation, a process that involves cortical F-actin disassembly. Actin depolymerization may be triggered by increase of cytosolic Ca2+. Entry of Ca2+ through the Ca2+ release-activated Ca2+ (CRAC) channels is under powerful regulation by the serum- and glucocorticoid-inducible kinase SGK1. Moreover, FceRI-dependent degranulation is decreased in SGK1-deficient (sgkl) MCs. The present study addressed whether SGK1 is required for actin cytoskeleton rearrangement in MCs and whether modulation of actin architecture could underlie decreased degranulation of sgkl MCs.
机译:高亲和力IgE受体(FceRI)在肥大细胞(MC)上的聚集会导致MC脱粒,该过程涉及皮质F-肌动蛋白的拆卸。肌动蛋白解聚可能是由胞质Ca2 +的增加触发的。通过Ca2 +释放激活的Ca2 +(CRAC)通道进入Ca2 +受血清和糖皮质激素诱导的激酶SGK1的强大调控。此外,在SGK1缺失(sgkl)MC中,依赖FceRI的脱粒减少。本研究解决了SGs中肌动蛋白细胞骨架重排是否需要SGK1,以及肌动蛋白结构的调节是否可以作为降低sgkl MC脱粒的基础。

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