Relaxin signalling in THP-1 cells uses a novel phosphotyrosine-dependent pathway
Relaxin signalling in THP-1 cells uses a novel phosphotyrosine-dependent pathway
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DOI：
10.1016/j.mce.2007.04.001
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发表时间：
2007-06-30
影响因子：
4.1
通讯作者：
Ivell, Richard
中科院分区：
文献类型：
--
作者：
Anand-Ivell, Ravinder;Heng, Kee;Ivell, Richard
异二聚体肽激素松弛素通过新型G蛋白偶联受体LGR 7起作用，以引发人单核细胞系THP-1中cAMP的产生。细胞表面上的受体数量非常少，并且细胞膜中缺乏反应，这意味着细胞质信号放大过程的参与。在这里，我们表明，这一过程包括一个新的和特定的酪氨酸激酶活性接近受体，既不涉及蛋白激酶A，促分裂原活化蛋白激酶，也不磷酸肌醇-3激酶的活动作为主要的上游组件。此外，这种酪氨酸激酶活性的新参与是细胞类型依赖性的，在LGR 7转染的HEK 293 T细胞中基本上不存在，并且是受体依赖性的;相同细胞中的血管活性肠肽或异丙肾上腺素信号传导不需要这种酪氨酸激酶活性。(C)2007爱思唯尔爱尔兰有限公司保留所有权利。
The heterodimeric peptide hormone relaxin acts through the novel G-protein coupled receptor LGR7 to elicit the production of cAMP in the human monocyte cell line THP-1. The very small number of receptors on the cell surface, and the lack of response in cell membranes imply the involvement of a cytoplasmic signal amplification process. Here we show that this process comprises a novel and specific tyrosine kinase activity close to the receptor, and involves neither protein kinase A, mitogen-activated protein kinase, nor phosphoinositide-3 kinase activities as major upstream components. Furthermore, this novel involvement of a tyrosine kinase activity is cell-type dependent, being largely absent from LGR7-transfected HEK293T cells, and receptor-dependent; vasoactive intestinal peptide or isoproterenol signalling in the same cells does not require this tyrosine kinase activity. (C) 2007 Elsevier Ireland Ltd. All rights reserved.