DEPLETION OF INSP3 STORES ACTIVATES A CA2+ AND K+ CURRENT BY MEANS OF A PHOSPHATASE AND A DIFFUSIBLE MESSENGER

DEPLETION OF INSP3 STORES ACTIVATES A CA2+ AND K+ CURRENT BY MEANS OF A PHOSPHATASE AND A DIFFUSIBLE MESSENGER
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DOI:
10.1038/364814a0
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发表时间:
1993-08-26
期刊:
影响因子:
64.8
通讯作者:
STUHMER, W
STUHMER, W
中科院分区:
综合性期刊1区
文献类型:
--
作者:
PAREKH, AB;TERLAU, H;STUHMER, W

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在非兴奋性细胞中,从肌醇1,4,5-三磷酸(InsP 3)-敏感的商店释放Ca 2+可以激活Ca 2+进入1 -3。很少有人知道有关的信号机制存储排空质膜Ca 2+内流。有人认为,信号可能是一个可扩散的信使,如磷酸肌醇4,或InsP 3受体本身,其中,通过物理耦合到质膜中的Ca 2+进入的一些组件,可以连接存储释放到Ca 2 + entry 5。Ca 2+进入途径的性质也不清楚。仅在肥大细胞中,在储存清空后观察到非常选择性的Ca 2+电流6。激活外源性5-羟色胺(5-HT)受体表达在非洲爪蟾卵母细胞或直接注射InsP 3引起钙离子进入激活InsP 3池耗尽7。在这里,我们调查的性质,这种流入途径,并发现激活池耗尽电流。这具有不寻常的选择性,因为它对Ca 2+离子比对其他二价阳离子(Ba 2+、Sr 2+或Mn 2+)更可渗透。此外,K+渗透性也被激发后池耗尽。这种存储耗尽电流的激活涉及磷酸酶和身份不明的扩散信使。在这里发现的Ca 2+进入途径和激活因子可能与各种非兴奋细胞中的池耗尽Ca 2+进入有关。
IN non-excitable cells, release of Ca2+ from the inositol 1,4,5-trisphosphate (InsP3)-sensitive store can activate Ca2+ entry1-3. Very little is known about the signal mechanism relating store emptying to plasma membrane Ca2+ influx. It has been suggested that the signal may be either a diffusible messenger like an inositol phosphate4, or the InsP3 receptor itself, which, by physically coupling to some component of Ca2+ entry in the plasma membrane, may link store release to Ca2+ entry5. The nature of the Ca2+ entry pathway is also unclear. Only in mast cells has a very selective Ca2+ current been observed after store emptying6. Activation of exogenous 5-hydroxytryptamine (5-HT) receptors expressed in Xenopus oocytes or direct injection of InsP3 evokes Ca2+ entry activated by InsP3 pool depletion7. Here we investigate the nature of this influx pathway and find a current activated by pool depletion. This has an unusual selectivity in that it is more permeable to Ca2+ ions than to other divalent cations (Ba2+, Sr2+ or Mn2+). Moreover, a K+ permeability is also stimulated after pool depletion. The activation of this store depletion current involves both a phosphatase and an unidentified diffusible messenger. Both the Ca2+ entry pathway and the activating factors found here may be relevant to pool-depleted Ca2+ entry in a variety of non-excitable cells.