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在癌细胞系中,AMP 激活的蛋白激酶的上调是通过 c-Src 的激活来介导的。

Up-regulation of AMP-activated protein kinase in cancer cell lines is mediated through c-Src activation.

机构信息

Unit of Cellular Signaling, Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel.

出版信息

J Biol Chem. 2011 Apr 29;286(17):15268-77. doi: 10.1074/jbc.M110.211813. Epub 2011 Jan 18.

DOI:10.1074/jbc.M110.211813
PMID:21245141
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3083231/
Abstract

We report that the activation level of AMP-dependent protein kinase AMPK is elevated in cancer cell lines as a hallmark of their transformed state. In OVCAR3 and A431 cells, c-Src signals through protein kinase Cα, phospholipase Cγ, and LKB1 to AMPK. AMPK controls internal ribosome entry site (IRES) dependent translation in these cells. We suggest that AMPK activation via PKC might be a general mechanism to regulate IRES-dependent translation in cancer cells.

摘要

我们报告称,作为其转化状态的标志,AMP 依赖的蛋白激酶 AMPK 的激活水平在癌细胞系中升高。在 OVCAR3 和 A431 细胞中,c-Src 通过蛋白激酶 Cα、磷脂酶 Cγ 和 LKB1 信号传递至 AMPK。AMPK 控制这些细胞中的内部核糖体进入位点(IRES)依赖的翻译。我们认为,PKC 介导的 AMPK 激活可能是调节癌细胞中 IRES 依赖翻译的一般机制。

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本文引用的文献

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Tumor suppressors and cell metabolism: a recipe for cancer growth.肿瘤抑制因子与细胞代谢:癌症生长的秘诀
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GIT1 mediates VEGF-induced podosome formation in endothelial cells: critical role for PLCgamma.GIT1介导血管内皮生长因子诱导内皮细胞中足体的形成:磷脂酶Cγ的关键作用。
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Phosphorylation of LKB1 at serine 428 by protein kinase C-zeta is required for metformin-enhanced activation of the AMP-activated protein kinase in endothelial cells.蛋白激酶C-ζ使LKB1的丝氨酸428位点磷酸化,这是二甲双胍增强内皮细胞中AMP激活的蛋白激酶活性所必需的。
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