STIMULATION OF CLONED HUMAN GLUCAGON-LIKE PEPTIDE-1 RECEPTOR EXPRESSED IN HEK-293 CELLS INDUCES CAMP-DEPENDENT ACTIVATION OF CALCIUM-INDUCED CALCIUM-RELEASE
STIMULATION OF CLONED HUMAN GLUCAGON-LIKE PEPTIDE-1 RECEPTOR EXPRESSED IN HEK-293 CELLS INDUCES CAMP-DEPENDENT ACTIVATION OF CALCIUM-INDUCED CALCIUM-RELEASE
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DOI：
10.1016/0014-5793(95)01070-u
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发表时间：
1995-10-09
期刊：
影响因子：
3.5
通讯作者：
WULFF, BS
中科院分区：
文献类型：
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作者：
GROMADA, J;RORSMAN, P;WULFF, BS
研究了胰高血糖素样肽-1（7-36）酰胺（GLP-1（7-36）酰胺）在稳定转染GLP-1受体的人胚胎肾293 （HEK 293）细胞中的信号传导作用。克隆的GLP-1受体具有单一高亲和力结合位点（K-d = 0.76 nM）。GLP-1（7-36）酰胺的结合以剂量依赖的方式刺激cAMP的产生（EC(50) = 0.015 nM），并引起细胞内游离Ca2+浓度的增加（[Ca2+](i)）。后一种效应反映Ca2+诱导的Ca2+释放，并被ryanodine抑制。我们提出GLP-1（7-36）酰胺增加[Ca2+]的能力(i)是由于通过蛋白激酶a依赖机制使ryanodine受体增敏。
The actions of glucagon-like peptide-1(7-36)amide (GLP-1(7-36)amide) on cellular signalling were studied in human embryonal kidney 293 (HEK 293) cells stably transfected with the cloned human GLP-1 receptor. The cloned GLP-1 receptor showed a single high-affinity binding site (K-d = 0.76 nM). Binding of GLP-1(7-36)amide stimulated cAMP production in a dose-dependent manner (EC(50) = 0.015 nM) and caused an increase in the intracellular free Ca2+ concentration ([Ca2+](i)). The latter effect reflected Ca2+-induced Ca2+ release and was suppressed by ryanodine. We propose that the ability of GLP-1(7-36)amide to increase [Ca2+](i) results from sensitization of the ryanodine receptors by a protein kinase A dependent mechanism.