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果蝇TRP和TRP样蛋白在非洲爪蟾卵母细胞中的共表达重构了容量性Ca2+内流。

Coexpression of Drosophila TRP and TRP-like proteins in Xenopus oocytes reconstitutes capacitative Ca2+ entry.

作者信息

Gillo B, Chorna I, Cohen H, Cook B, Manistersky I, Chorev M, Arnon A, Pollock J A, Selinger Z, Minke B

机构信息

Department of Physiology, Hebrew University, Jerusalem, Israel.

出版信息

Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):14146-51. doi: 10.1073/pnas.93.24.14146.

DOI:10.1073/pnas.93.24.14146
PMID:8943075
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC19508/
Abstract

Capacitative Ca2+ entry is a component of the inositol-lipid signaling in which depletion of inositol 1,4,5-trisphosphate (InsP3)-sensitive Ca2+ stores activates Ca2+ influx by a mechanism that is still unknown. This pathway plays a central role in cellular signaling, which is mediated by many hormones, neurotransmitters, and growth factors. Studies of Drosophila photoreceptors provided the first putative capacitative Ca2+ entry mutant designated transient receptor potential (trp) and a Drosophila gene encoding TRP-like protein (trpl). It is not clear how the Ca2+ store depletion signal is relayed to the plasma membrane and whether both TRP and TRPL participate in this process. We report here that coexpressing Drosophila TRP and TRPL in Xenopus oocytes synergistically enhances the endogenous Ca(2+)-activated Cl- current and produces a divalent inward current. Both of these currents are activated by Ca2+ store depletion. In the absence of Ca2+, Mg2+ is the main charge carrier of the divalent current. This current is characterized by lanthanum sensitivity and a voltage-dependent blocking effect of Mg2+, which is relieved at both hyperpolarizing (inward rectification) and depolarizing (outward rectification) potentials. The store-operated divalent current is neither observed in native oocytes nor in oocytes expressing either TRP or TRPL alone. The production of this current implicates a cooperative action of TRP and TRPL in the depletion-activated current.

摘要

容量性钙离子内流是肌醇磷脂信号传导的一个组成部分,其中肌醇1,4,5-三磷酸(InsP3)敏感的钙离子储存库的耗竭通过一种仍不清楚的机制激活钙离子内流。这条途径在细胞信号传导中起核心作用,细胞信号传导由许多激素、神经递质和生长因子介导。对果蝇光感受器的研究提供了第一个假定的容量性钙离子内流突变体,命名为瞬时受体电位(trp),以及一个编码TRP样蛋白的果蝇基因(trpl)。目前尚不清楚钙离子储存库耗竭信号是如何传递到质膜的,以及TRP和TRPL是否都参与了这一过程。我们在此报告,在非洲爪蟾卵母细胞中共表达果蝇TRP和TRPL可协同增强内源性钙离子激活的氯离子电流,并产生二价内向电流。这两种电流均由钙离子储存库耗竭激活。在没有钙离子的情况下,镁离子是二价电流的主要电荷载体。该电流的特征是对镧敏感以及镁离子的电压依赖性阻断效应,在超极化(内向整流)和去极化(外向整流)电位下该效应均会解除。在天然卵母细胞或单独表达TRP或TRPL的卵母细胞中均未观察到储存库操纵的二价电流。这种电流的产生暗示了TRP和TRPL在耗竭激活电流中的协同作用。

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Coexpression of Drosophila TRP and TRP-like proteins in Xenopus oocytes reconstitutes capacitative Ca2+ entry.果蝇TRP和TRP样蛋白在非洲爪蟾卵母细胞中的共表达重构了容量性Ca2+内流。
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