The calcium-sensing receptor stimulates JNK in MDCK cells
The calcium-sensing receptor stimulates JNK in MDCK cells
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DOI：
10.1006/bbrc.2000.3226
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发表时间：
2000-08-28
影响因子：
3.1
通讯作者：
McLeish, KR
中科院分区：
文献类型：
--
作者：
Arthur, JM;Lawrence, MS;McLeish, KR
钙敏感受体(CAR)刺激大鼠成纤维细胞中的ERK1，但其对其他MAP激酶的作用尚不清楚。我们使用了一个肾脏远端小管的模型，即MDCK细胞，来确定CALL的效果。对Jun激酶(JNK)活性的刺激。5 mM Ca~(2+)刺激后，JNK活性呈时间依赖性增加。JNK的激活优先于刺激基底面而不是根尖面。基础应用CAR激动剂Gd(30微米)也能刺激JNK活性。百日咳毒素阻断两种CAR激动剂刺激JNK的能力，表明其作用是通过G(Iα)类G蛋白介导的。最后，我们使用共聚焦显微镜来确定CAR主要位于基底表面。这些研究首次证明，CAR能刺激JNK活性。(C)2000年学术出版社。
The calcium-sensing receptor (CaR) stimulates ERK1 in rat fibroblasts, but its effect on other MAP kinases is not known. We used a model of renal distal tubule, the MDCK cell, to determine the effects of Call. stimulation on Jun kinase (JNK) activity. Stimulation of the Call with 5 mM Ca2+ resulted in a time-dependent increase in JNK activity. Activation of JNK occurred preferentially with stimulation on the basal surface relative to the apical surface. Basal administration of the CaR agonist gadolinium (30 mu m) also stimulated JNK activity. Pertussis toxin blocked the ability of both CaR agonists to stimulate JNK, indicating that the effect was mediated through G(i alpha) class G proteins. Finally, we used confocal microscopy to determine that the CaR was located predominantly on the basal surface. These studies demonstrate for the first time that the CaR stimulates JNK activity. (C) 2000 Academic Press.