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Biochem J. 2006 Sep 1;398(2):243-56. doi: 10.1042/BJ20060160.

本文引用的文献

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Gab1 is required for EGF receptor signaling and the transformation by activated ErbB2.Gab1是表皮生长因子（EGF）受体信号传导以及由激活的ErbB2介导的细胞转化所必需的。
Oncogene. 2003 Mar 13;22(10):1546-56. doi: 10.1038/sj.onc.1206284.
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Lysophosphatidic acid-regulated mitogenic ERK signaling in androgen-insensitive prostate cancer PC-3 cells.溶血磷脂酸调节雄激素不敏感前列腺癌PC-3细胞中的有丝分裂原性细胞外信号调节激酶信号通路。
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Lysophosphatidic acid-induced squamous cell carcinoma cell proliferation and motility involves epidermal growth factor receptor signal transactivation.溶血磷脂酸诱导的鳞状细胞癌细胞增殖和迁移涉及表皮生长因子受体信号转活化。
Cancer Res. 2002 Nov 1;62(21):6329-36.
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A function for phosphoinositide 3-kinase beta lipid products in coupling beta gamma to Ras activation in response to lysophosphatidic acid.磷脂酰肌醇3-激酶β脂质产物在响应溶血磷脂酸时将βγ与Ras激活偶联中的作用。
J Biol Chem. 2002 Jun 14;277(24):21167-78. doi: 10.1074/jbc.M110411200. Epub 2002 Mar 26.
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A dual signaling cascade that regulates the ectodomain shedding of heparin-binding epidermal growth factor-like growth factor.一种调节肝素结合表皮生长因子样生长因子胞外域脱落的双信号级联反应。
J Biol Chem. 2001 Aug 10;276(32):30475-82. doi: 10.1074/jbc.M103673200. Epub 2001 Jun 11.
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beta-Migrating very low density lipoprotein (beta VLDL) activates smooth muscle cell mitogen-activated protein (MAP) kinase via G protein-coupled receptor-mediated transactivation of the epidermal growth factor (EGF) receptor: effect of MAP kinase activation on beta VLDL plus EGF-induced cell proliferation.β迁移极低密度脂蛋白（β-VLDL）通过G蛋白偶联受体介导的表皮生长因子（EGF）受体反式激活来激活平滑肌细胞丝裂原活化蛋白（MAP）激酶：MAP激酶激活对β-VLDL加EGF诱导的细胞增殖的影响。
J Biol Chem. 2001 Aug 17;276(33):30579-88. doi: 10.1074/jbc.M103761200. Epub 2001 May 25.
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Thrombin-induced p38 mitogen-activated protein kinase activation is mediated by epidermal growth factor receptor transactivation pathway.凝血酶诱导的p38丝裂原活化蛋白激酶激活是由表皮生长因子受体反式激活途径介导的。
Br J Pharmacol. 2001 Apr;132(8):1657-64. doi: 10.1038/sj.bjp.0703952.
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Src and Pyk2 mediate G-protein-coupled receptor activation of epidermal growth factor receptor (EGFR) but are not required for coupling to the mitogen-activated protein (MAP) kinase signaling cascade.Src和Pyk2介导G蛋白偶联受体对表皮生长因子受体（EGFR）的激活，但对于与丝裂原活化蛋白（MAP）激酶信号级联的偶联并非必需。
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A permissive function of phosphoinositide 3-kinase in Ras activation mediated by inhibition of GTPase-activating proteins.
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Transactivation of the EGF receptor mediates IGF-1-stimulated shc phosphorylation and ERK1/2 activation in COS-7 cells.表皮生长因子（EGF）受体的反式激活介导了胰岛素样生长因子-1（IGF-1）刺激的COS-7细胞中Shc磷酸化及细胞外信号调节激酶1/2（ERK1/2）的激活。
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溶血磷脂酸诱导的Ras激活需要来自表皮生长因子受体的允许性输入。

Ras activation in response to lysophosphatidic acid requires a permissive input from the epidermal growth factor receptor.

作者信息

Rubio Ignacio, Rennert Knut, Wittig Ute, Wetzker Reinhard

机构信息

Institute of Molecular Cell Biology, Medical Faculty, Friedrich-Schiller-University, Drackendorfer Strasse 1, 07747 Jena, Germany.

出版信息

Biochem J. 2003 Dec 15;376(Pt 3):571-6. doi: 10.1042/BJ20031410.

DOI:10.1042/BJ20031410
PMID:14580235
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1223827/
Abstract

The topology of the signalling pathway linking the G-protein-coupled receptor agonist lysophosphatidic acid (LPA) to extracellular-signal-regulated kinase activation remains undeciphered. In the present study, we report that analysis of LPA signals at the level of Ras-GTP formation and Ras nucleotide exchange discriminates true mediatory signals from permissive activities that do not participate in signal relay. Hence, whereas pertussis toxin (PTX) treatment impairs stimulation of nucleotide exchange, epidermal growth factor receptor (EGFR) inhibition does not compromise LPA-induced acceleration of nucleotide exchange, but instead attenuates basal nucleotide turnover on Ras. Our data indicate that LPA activation of Ras proceeds via PTX-sensitive G(i/o)-proteins and requires a permissive input from basal EGFR activity.

摘要

将G蛋白偶联受体激动剂溶血磷脂酸（LPA）与细胞外信号调节激酶激活相联系的信号通路拓扑结构仍未被破解。在本研究中，我们报告称，在Ras-GTP形成和Ras核苷酸交换水平上对LPA信号进行分析，可区分真正的介导信号与不参与信号传递的允许性活动。因此，尽管百日咳毒素（PTX）处理会损害核苷酸交换的刺激，但表皮生长因子受体（EGFR）抑制并不会损害LPA诱导的核苷酸交换加速，反而会减弱Ras上的基础核苷酸周转。我们的数据表明，LPA对Ras的激活通过对PTX敏感的G(i/o)蛋白进行，并且需要基础EGFR活性的允许性输入。