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Phosphatidylinositol 3-kinase/Akt pathway targets acetylation of Smad3 through Smad3/CREB-binding protein interaction: contribution to transforming growth factor beta1-induced Epstein-Barr virus reactivation.磷脂酰肌醇3激酶/蛋白激酶B通路通过Smad3/ CREB结合蛋白相互作用靶向Smad3的乙酰化：对转化生长因子β1诱导的爱泼斯坦-巴尔病毒激活的作用
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The phosphatidylinositol 3-kinase/Akt pathway enhances Smad3-stimulated mesangial cell collagen I expression in response to transforming growth factor-beta1.磷脂酰肌醇3激酶/蛋白激酶B信号通路增强了Smad3刺激的系膜细胞I型胶原蛋白表达，以响应转化生长因子-β1。
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本文引用的文献

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Epstein-Barr virus upregulates phosphorylated heat shock protein 27 kDa in carcinoma cells using the phosphoinositide 3-kinase/Akt pathway.爱泼斯坦-巴尔病毒通过磷酸肌醇3-激酶/蛋白激酶B信号通路在癌细胞中上调磷酸化的27 kDa热休克蛋白。
Electrophoresis. 2008 Aug;29(15):3192-200. doi: 10.1002/elps.200800086.
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Akt kinase targets association of CBP with SMAD 3 to regulate TGFbeta-induced expression of plasminogen activator inhibitor-1.Akt激酶靶向CBP与SMAD 3的结合，以调节转化生长因子β诱导的纤溶酶原激活物抑制剂-1的表达。
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p38 MAPK and MSK1 mediate caspase-8 activation in manganese-induced mitochondria-dependent cell death.
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Smad3 is acetylated by p300/CBP to regulate its transactivation activity.Smad3 被 p300/CBP 乙酰化以调节其反式激活活性。
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Tumour microenvironment: TGFbeta: the molecular Jekyll and Hyde of cancer.肿瘤微环境：转化生长因子β：癌症的分子双重人格
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Epstein-Barr virus (EBV) genome and expression in breast cancer tissue: effect of EBV infection of breast cancer cells on resistance to paclitaxel (Taxol).爱泼斯坦-巴尔病毒（EBV）基因组及其在乳腺癌组织中的表达：EBV感染乳腺癌细胞对紫杉醇（泰素）耐药性的影响
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Transforming growth factor-beta activation of phosphatidylinositol 3-kinase is independent of Smad2 and Smad3 and regulates fibroblast responses via p21-activated kinase-2.转化生长因子-β 激活磷脂酰肌醇 3-激酶不依赖 Smad2 和 Smad3，并通过 p21 激活激酶-2 调节成纤维细胞反应。
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Epstein-Barr virus lytic infection contributes to lymphoproliferative disease in a SCID mouse model.在一种严重联合免疫缺陷（SCID）小鼠模型中，爱泼斯坦-巴尔病毒的裂解感染会导致淋巴增殖性疾病。
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Identification of N10-substituted phenoxazines as potent and specific inhibitors of Akt signaling.鉴定N10-取代吩恶嗪为Akt信号通路的有效且特异性抑制剂。
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Histone acetyltransferase activity of p300 is required for transcriptional repression by the promyelocytic leukemia zinc finger protein.早幼粒细胞白血病锌指蛋白介导的转录抑制需要p300的组蛋白乙酰转移酶活性。
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磷脂酰肌醇3激酶/蛋白激酶B通路通过Smad3/ CREB结合蛋白相互作用靶向Smad3的乙酰化：对转化生长因子β1诱导的爱泼斯坦-巴尔病毒激活的作用

Phosphatidylinositol 3-kinase/Akt pathway targets acetylation of Smad3 through Smad3/CREB-binding protein interaction: contribution to transforming growth factor beta1-induced Epstein-Barr virus reactivation.

作者信息

Oussaief Lassad, Hippocrate Aurélie, Ramirez Vanessa, Rampanou Aurore, Zhang Wei, Meyers David, Cole Philip, Khelifa Ridha, Joab Irène

机构信息

UMR542 INSERM-Université Paris 11, Hôpital Paul Brousse, 94807 Villejuif Cedex, France.

出版信息

J Biol Chem. 2009 Sep 4;284(36):23912-24. doi: 10.1074/jbc.M109.036483. Epub 2009 Jul 9.

DOI:10.1074/jbc.M109.036483
PMID:19589780
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2781985/
Abstract

Epstein-Barr virus, a ubiquitous human herpesvirus, is associated with the development of carcinomas and lymphomas. We previously showed that transforming growth factor beta1 (TGF-beta1) mediated the virus to enter the lytic cycle, which is triggered by expression of Z Epstein-Barr virus replication activator (ZEBRA), through the ERK 1/2 MAPK signaling pathway. We report here that Akt, activated downstream from ERK 1/2, was required for TGF-beta1-induced ZEBRA expression and enabled Smad3, a mediator of TGF-beta1 signaling, to be acetylated by direct interaction with the co-activator CREB-binding protein and then to regulate TGF-beta1-induced ZEBRA expression.

摘要

爱泼斯坦-巴尔病毒是一种普遍存在的人类疱疹病毒，与癌和淋巴瘤的发生有关。我们之前表明，转化生长因子β1（TGF-β1）通过ERK 1/2丝裂原活化蛋白激酶信号通路介导病毒进入裂解周期，该周期由Z爱泼斯坦-巴尔病毒复制激活因子（ZEBRA）的表达触发。我们在此报告，ERK 1/2下游被激活的Akt是TGF-β1诱导ZEBRA表达所必需的，并且使TGF-β1信号传导的介质Smad3通过与共激活因子CREB结合蛋白直接相互作用而被乙酰化，进而调节TGF-β1诱导的ZEBRA表达。