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爱泼斯坦-巴尔病毒核抗原3C对细胞周期机制的失调作用

Deregulation of the cell cycle machinery by Epstein-Barr virus nuclear antigen 3C.

作者信息

Kumar Pankaj, Murakami Masanao, Kaul Rajeev, Saha Abhik, Cai Qiliang, Robertson Erle S

机构信息

Department of Microbiology & The Tumor Virology Program of the Abramson Comprehensive Cancer Center, University of Pennsylvania School of Medicine, PA, USA.

Department of Microbiology & The Tumor Virology Program of the Abramson Comprehensive Cancer Center, University of Pennsylvania School of Medicine, 201E Johnson Pavilion, 3610 Hamilton Walk, Philadelphia, PA 19104, USA, Tel.: +1 215 746 0114;

出版信息

Future Virol. 2009 Jan;4(1):79-91. doi: 10.2217/17460794.4.1.79.

DOI:10.2217/17460794.4.1.79
PMID:25635182
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4307939/
Abstract

Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus associated with a large number of lymphoid and epithelial malignancies. As a successful pathogen it has co-evolved with its human host for millions of years. EBV has the unique ability to establish life-long latent infection in primary human B lymphocytes. During latent infection, a small subset of viral proteins is expressed. These proteins are essential for maintenance of the EBV genome as well as the deregulation of various signaling pathways that facilitate the proliferation and survival of the infected cells. Epstein-Barr nuclear antigen (EBNA)3C is one of the latent proteins shown to be essential for transformation of primary human B lymphocytes . EBNA3C primarily functions as a transcriptional regulator by interacting with a number of well known cellular and viral transcriptional factors. We have recently identified several binding partners for EBNA3C including proteins that regulate cell cycle and chromatin remodeling. We are actively engaged in discerning the biological significance of these interactions. This review summarizes our current understanding of how EBNA3C usurps cellular pathways that promote B-cell transformation.

摘要

爱泼斯坦-巴尔病毒(EBV)是一种普遍存在的人类疱疹病毒,与大量淋巴和上皮恶性肿瘤相关。作为一种成功的病原体,它已经与人类宿主共同进化了数百万年。EBV具有在原代人类B淋巴细胞中建立终身潜伏感染的独特能力。在潜伏感染期间,一小部分病毒蛋白会表达。这些蛋白对于维持EBV基因组以及失调促进受感染细胞增殖和存活的各种信号通路至关重要。爱泼斯坦-巴尔核抗原(EBNA)3C是一种潜伏蛋白,已被证明对原代人类B淋巴细胞的转化至关重要。EBNA3C主要通过与许多知名的细胞和病毒转录因子相互作用来发挥转录调节因子的作用。我们最近鉴定了EBNA3C的几个结合伙伴,包括调节细胞周期和染色质重塑的蛋白。我们正在积极致力于识别这些相互作用的生物学意义。这篇综述总结了我们目前对EBNA3C如何篡夺促进B细胞转化的细胞途径的理解。

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本文引用的文献

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EBV-encoded EBNA-6 binds and targets MRS18-2 to the nucleus, resulting in the disruption of pRb-E2F1 complexes.爱泼斯坦-巴尔病毒(EBV)编码的EBNA-6与MRS18-2结合并将其靶向细胞核,导致视网膜母细胞瘤蛋白(pRb)-E2F1复合物的破坏。
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Epstein-Barr virus nuclear antigen 3C interacts with and enhances the stability of the c-Myc oncoprotein.爱泼斯坦-巴尔病毒核抗原3C与c-Myc癌蛋白相互作用并增强其稳定性。
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Two Epstein-Barr virus (EBV) oncoproteins cooperate to repress expression of the proapoptotic tumour-suppressor Bim: clues to the pathogenesis of Burkitt's lymphoma.两种爱泼斯坦-巴尔病毒(EBV)癌蛋白协同抑制促凋亡肿瘤抑制因子Bim的表达:伯基特淋巴瘤发病机制的线索
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The ATM/ATR signaling effector Chk2 is targeted by Epstein-Barr virus nuclear antigen 3C to release the G2/M cell cycle block.ATM/ATR信号传导效应因子Chk2是爱泼斯坦-巴尔病毒核抗原3C的作用靶点,用于解除G2/M期细胞周期阻滞。
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Epstein-Barr virus nuclear protein EBNA3C is required for cell cycle progression and growth maintenance of lymphoblastoid cells.爱泼斯坦-巴尔病毒核蛋白EBNA3C是淋巴母细胞的细胞周期进程和生长维持所必需的。
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