Regulation of the retinoblastoma proteins by the human herpesviruses.
Regulation of the retinoblastoma proteins by the human herpesviruses.
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DOI：
10.1186/1747-1028-4-1
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发表时间：
2009-01-15
期刊：
影响因子：
2.3
通讯作者：
Kalejta RF
中科院分区：
文献类型：
--
作者：
Hume AJ;Kalejta RF
病毒是专性细胞内寄生虫，其改变受感染细胞的环境以更有效地复制。病毒实现这一点的一种方式是通过调节细胞周期进程。从G 0期到G1期再到S期的主要调控因子是肿瘤抑制因子视网膜母细胞瘤（Rb）家族的成员。Rb蛋白抑制由E2 F转录因子控制的基因的转录。由于E2 F反应基因的表达是细胞周期进入S期所必需的，Rb将细胞周期阻滞在G 0/G1期。许多病毒蛋白直接靶向Rb家族成员进行失活，可能是为了创造一个更适合病毒复制的环境。这些病毒蛋白包括广泛研究的癌蛋白E7（来自人乳头瘤病毒），E1 A（来自腺病毒）和大T（肿瘤）抗原（来自猿猴病毒40）。阐明这三种病毒蛋白如何靶向和靶向Rb已被证明是一种非常宝贵的方法，以增加我们对正常细胞周期进程和致癌作用的理解。除了这些蛋白质之外，随后还鉴定了Rb家族的许多其他病毒编码的灭活剂，包括由人类疱疹病毒编码的令人惊讶的数量。在这里，我们回顾了人类疱疹病毒如何调节Rb的功能，在感染过程中，介绍了个别病毒蛋白，直接或间接靶向Rb，并推测Rb调制这些蛋白可能发挥什么作用，在病毒复制，发病机制和肿瘤发生。
Viruses are obligate intracellular parasites that alter the environment of infected cells in order to replicate more efficiently. One way viruses achieve this is by modulating cell cycle progression. The main regulators of progression out of G0, through G1, and into S phase are the members of the retinoblastoma (Rb) family of tumor suppressors. Rb proteins repress the transcription of genes controlled by the E2F transcription factors. Because the expression of E2F-responsive genes is required for cell cycle progression into the S phase, Rb arrests the cell cycle in G0/G1. A number of viral proteins directly target Rb family members for inactivation, presumably to create an environment more hospitable for viral replication. Such viral proteins include the extensively studied oncoproteins E7 (from human papillomavirus), E1A (from adenovirus), and the large T (tumor) antigen (from simian virus 40). Elucidating how these three viral proteins target and inactivate Rb has proven to be an invaluable approach to augment our understanding of both normal cell cycle progression and carcinogenesis. In addition to these proteins, a number of other virally-encoded inactivators of the Rb family have subsequently been identified including a surprising number encoded by human herpesviruses. Here we review how the human herpesviruses modulate Rb function during infection, introduce the individual viral proteins that directly or indirectly target Rb, and speculate about what roles Rb modulation by these proteins may play in viral replication, pathogenesis, and oncogenesis.
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