Ca2+ entry through plasma membrane IP3 receptors

被引：152

作者：

Dellis, Olivier ^{[1
]}

Dedos, Skarlatos G. ^{[1
]}

Tovey, Stephen C. ^{[1
]}

Taufiq-Ur-Rahman ^{[1
]}

Dubel, Stefan J. ^{[1
]}

Taylor, Colin W. ^{[1
]}

机构：

[1] Dept Pharmacol, Cambridge CB2 1PD, England

来源：

SCIENCE | 2006年 / 313卷 / 5784期

基金：

英国生物技术与生命科学研究理事会; 英国惠康基金;

关键词：

D O I：

10.1126/science.1125203

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页码：229 / 233

页数：5

共 28 条

[1] INOSITOL TRISPHOSPHATE AND CALCIUM SIGNALING [J].