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由免疫球蛋白E受体交联激活的钙通道的初步特性研究

Initial characterization of the calcium channel activated by the cross-linking of the receptors for immunoglobulin E.

作者信息

Kanner B I, Metzger H

出版信息

J Biol Chem. 1984 Aug 25;259(16):10188-93.

PMID:6088486
Abstract

It is currently thought that aggregation of the receptor for immunoglobulin E on mast cells, basophils, and a tumor analog, rat basophilic leukemia (RBL) cells, induces an enhanced permeability of the plasma membrane to calcium, thereby initiating degranulation of the cells. Even in the absence of calcium ions, aggregation of the receptor causes depolarization of the plasma membrane (Kanner, B. I., and Metzger, H. (1983) Proc. Natl. Acad. Sci. U. S. A. 80, 5744-5748), suggesting that other ions can traverse the putative channel. Direct evidence for this now has been obtained with measurements of increased 22Na+ fluxes in the absence of calcium ions, induced by aggregation of receptors. This reaction was optimally studied in the presence of ouabain. When aggregation of the receptor was induced by reacting the cell-bound IgE with a multivalent antigen, the sodium flux was completely inhibited by univalent hapten. The sodium flux was also completely inhibited by 2 mM calcium. Aggregation-induced 45Ca2+ fluxes were observed in the presence of millimolar concentrations of external Ca2+, but not in its absence. Depolarization of the plasma membrane potential by the addition of potassium to the medium in the presence of calcium did not itself induce degranulation. In fact, aggregation of the receptors for IgE in the presence of high external potassium resulted in a greatly diminished degranulation. These data indicate that the ion channel modulated by aggregation of receptor differs from the voltage-dependent type of calcium channels. We suggest that in the absence of calcium this channel is rather unspecific, but that calcium can modify it to become calcium selective.

摘要

目前认为,免疫球蛋白E在肥大细胞、嗜碱性粒细胞以及一种肿瘤类似物大鼠嗜碱性白血病(RBL)细胞上的受体聚集,会导致质膜对钙的通透性增强,从而引发细胞脱颗粒。即使在没有钙离子的情况下,受体聚集也会导致质膜去极化(坎纳,B.I.,和梅茨格,H.(1983年)《美国国家科学院院刊》80,5744 - 5748),这表明其他离子可以穿过假定的通道。现在通过测量在没有钙离子的情况下受体聚集诱导的22Na +通量增加,已经获得了这方面的直接证据。在哇巴因存在的情况下对该反应进行了最佳研究。当通过使细胞结合的IgE与多价抗原反应诱导受体聚集时,单价半抗原可完全抑制钠通量。2 mM钙也可完全抑制钠通量。在存在毫摩尔浓度的外部Ca2 +时观察到聚集诱导的45Ca2 +通量,但在没有外部Ca2 +时则未观察到。在有钙的情况下向培养基中添加钾使质膜电位去极化本身并不会诱导脱颗粒。事实上,在高外部钾存在的情况下IgE受体的聚集导致脱颗粒大大减少。这些数据表明,由受体聚集调节的离子通道不同于电压依赖性钙通道类型。我们认为,在没有钙的情况下,该通道相当非特异性,但钙可以使其发生改变以变得对钙具有选择性。

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