Ca2+ entry through plasma membrane IP3 receptors
Ca2+ entry through plasma membrane IP3 receptors
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DOI：
10.1126/science.1125203
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发表时间：
2006-07-14
期刊：
影响因子：
56.9
通讯作者：
Taylor, Colin W.
中科院分区：
文献类型：
--
作者：
Dellis, Olivier;Dedos, Skarlatos G.;Taylor, Colin W.
肌醇1，4，5-三磷酸受体（IP（3）Rs）从细胞内释放钙离子，但它们在介导钙内流中的作用尚不清楚。在DT 40鸡或小鼠B细胞的全细胞膜片钳记录中，IP 3刺激非常少的（每个细胞1.9 +/- 0.2个）Ca 2+渗透通道的开放。在穿孔贴片记录中激活B细胞受体（BCR）也引起了同样的反应。在缺乏IP 3 R的细胞中，IP 3不能刺激细胞内或质膜（PM）通道。IP 3R的表达恢复了这两种反应。孔内的突变同样影响IP 3激活的PM和细胞内通道的电导。不渗透孔突变体消除了BCR诱发的Ca 2+信号，PM IP（3）Rs检测不到。在孔附近引入α-银环蛇毒素结合位点后，PM IP（3）Rs受到细胞外α-银环蛇毒素的调节。在内质网蛋白中，IP（3）R也在PM功能性表达，这是不寻常的，在PM中，很少有IP（3）R对BCR诱发的Ca 2+内流有实质性贡献。
Inositol 1,4,5-trisphosphate receptors (IP(3)Rs) release calcium ions, Ca2+, from intracellular stores, but their roles in mediating Ca2+ entry are unclear. IP3 stimulated opening of very few (1.9 +/- 0.2 per cell) Ca2+-permeable channels in whole-cell patch-clamp recording of DT40 chicken or mouse B cells. Activation of the B cell receptor (BCR) in perforated-patch recordings evoked the same response. IP3 failed to stimulate intracellular or plasma membrane ( PM) channels in cells lacking IP3 R. Expression of IP3R restored both responses. Mutations within the pore affected the conductances of IP3-activated PM and intracellular channels similarly. An impermeant pore mutant abolished BCR-evoked Ca2+ signals, and PM IP(3)Rs were undetectable. After introduction of an alpha-bungarotoxin binding site near the pore, PM IP(3)Rs were modulated by extracellular alpha-bungarotoxin. IP(3)Rs are unusual among endoplasmic reticulum proteins in being also functionally expressed at the PM, where very few IP(3)Rs contribute substantially to the Ca2+ entry evoked by the BCR.