Division of Infectious Disease Biology, Institute of Life Sciences, Nalco Square, Chandrasekharpur, Bhubaneswar 751023, India.
Virology. 2014 Jan 5;448:333-43. doi: 10.1016/j.virol.2013.10.023. Epub 2013 Nov 12.
The p73 protein has structural and functional homology with the tumor suppressor p53, which plays an important role in cell cycle regulation, apoptosis, and DNA repair. The p73 locus encodes both a tumor suppressor (TAp73) and a putative oncogene (ΔNp73). p73 May play a significant role in p53-deficient lymphomas infected with Epstein-Barr virus (EBV). EBV produces an asymptomatic infection in the majority of the global population, but it is associated with several human B-cell malignancies. The EBV-encoded Epstein-Barr virus nuclear antigen 3C (EBNA3C) is thought to disrupt the cell cycle checkpoint by interacting directly with p53 family proteins. Doxorubicin, a commonly used chemotherapeutic agent, induces apoptosis through p53 and p73 signaling such that the lowΔNp73 level promotes the p73-mediated intrinsic pathway of apoptosis. In this report, we investigated the mechanism by which EBV infection counters p73α-induced apoptosis through EBNA3C.
p73 蛋白与肿瘤抑制因子 p53 具有结构和功能上的同源性，p53 在细胞周期调控、细胞凋亡和 DNA 修复中发挥着重要作用。p73 基因座编码两种蛋白：一种是肿瘤抑制因子（TAp73），另一种是假定的癌基因（ΔNp73）。p73 在感染 EBV 的 p53 缺陷型淋巴瘤中可能发挥重要作用。EBV 在全球大多数人群中引发无症状感染，但它与几种人类 B 细胞恶性肿瘤有关。EBV 编码的 Epstein-Barr 病毒核抗原 3C（EBNA3C）被认为通过与 p53 家族蛋白直接相互作用破坏细胞周期检查点。多柔比星是一种常用的化疗药物，通过 p53 和 p73 信号诱导细胞凋亡，因此低水平的 ΔNp73 促进 p73 介导的细胞凋亡内在途径。在本报告中，我们研究了 EBV 感染通过 EBNA3C 拮抗 p73α诱导的细胞凋亡的机制。
