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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Activation of calcium entry in human carcinoma A431 cells by store depletion and phospholipase C- dependent mechanisms converge on I_CRAC-like calcium channels
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Activation of calcium entry in human carcinoma A431 cells by store depletion and phospholipase C- dependent mechanisms converge on I_CRAC-like calcium channels

机译：通过储存耗竭和磷脂酶C依赖性机制激活人癌A431细胞中钙进入的激活收敛于I_CRAC样钙通道

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摘要

Activation of phospholipase C in nonexcitable cells causes the release of calcium (Ca~2+) from intracellular stores and activation of Ca~2+ influx by means of Ca~2+ release-activated channels (I_CRAC) in the plasma membrane. The molecular identity and the mechanism of I_CRAC channel activation are poorly understood. Using the patch--clamp technique, here we describe the plasma membrane Ca~2+ channels in human carcinoma A431 cells, which can be activated by extracellular UTP. by depletion of intracellular Ca~2+ stores after exposure to the Ca~2+-pump inhibitor thapsigargin, or by loading the cells with Ca~2+ chelator 1,2-bis(2-aminophe- noxy)ethane-N,N,N',N'-tetraacetat The observed channels dis- play the same conductance and gating properties as previously described I_min channels, but have significantly lower conductance for monovalent cations than the I_CRAC channels. Thus. we con- cluded that the depletion-activated Ca~2+ current in A431 cells is supported by I_CRAC-like (ICRACL) channels, identical to I_min.We further demonstrated synergism in activation of I_CRACL Ca~2+ chan- nels by extracellular UTP and intracellular inositol (1,4,5)-triphos- phate (IP3), apparently because of reduction in phosphatidylinosi- tol 4,5-bisphosphate (PIP_2) levels in the patch. Prolonged exposure of patches to thapsigargin renders I_CRACL Ca~2+ channels unrespon- sive to IP3 but still available to activation by the combined action of IP_3 and anti-PIP_2 antibody. Based on these data, we concluded that phospholipase C-mediated and store-operated Ca~2+ influx pathways in A431 cells converge on the same I_CRACL Ca~2+ channel. which can be modulated by PIP_2.
机译：不可激活细胞中磷脂酶C的激活导致钙（Ca〜2 +）从细胞内储存中释放出来，并通过质膜中的Ca〜2 +释放激活通道（I_CRAC）激活Ca〜2 +流入。分子身份和I_CRAC通道激活的机制了解甚少。在这里，我们使用膜片钳技术描述人癌细胞A431细胞中的质膜Ca〜2 +通道，该通道可以被细胞外UTP激活。通过暴露于Ca〜2 +泵抑制剂thapsigargin后耗尽细胞内Ca〜2 +储备，或通过向细胞中加入Ca〜2 +螯合剂1,2-双（2-氨基苯氧基）乙烷-N，N ，N'，N'-四乙酸盐观察到的通道具有与先前描述的I_min通道相同的电导率和门控特性，但单价阳离子的电导率明显低于I_CRAC通道。从而。我们认为A431细胞中的耗尽激活Ca〜2 +电流受I_CRAC样（ICRACL）通道支持，与I_min相同。我们进一步证明了细胞外UTP激活I_CRACL Ca〜2 +通道的协同作用。以及细胞内肌醇（1,4,5）-三磷酸（IP3），显然是因为该贴片中的磷脂酰肌醇4,5-二磷酸（PIP_2）水平降低。膜片长时间暴露于毒胡萝卜素使I_CRACL Ca〜2 +通道对IP3无反应，但仍可通过IP_3和抗PIP_2抗体的联合作用激活。根据这些数据，我们得出结论，A431细胞中磷脂酶C介导的和由存储操作的Ca〜2 +内流途径收敛于同一I_CRACL Ca〜2 +通道。可以通过PIP_2进行调制。

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