Polster Brian M, Pevsner Jonathan, Hardwick J Marie
W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Biochim Biophys Acta. 2004 Mar 1;1644(2-3):211-27. doi: 10.1016/j.bbamcr.2003.11.001.
Cellular Bcl-2 family proteins regulate a critical step in the mammalian programmed cell death pathway by modulating mitochondrial permeability and function. Bcl-2 family proteins are also encoded by several large DNA viruses, including all known gamma herpesviruses, adenoviruses, and several other unrelated viruses. Viral Bcl-2 proteins can prevent cell death but often escape cellular regulatory mechanisms that govern their cellular counterparts. By evading the "altruistic" suicide of infected cells, viruses can ensure replication and propagation in the infected host, but sometimes in surprising ways. Many human cancers and other disorders are associated with viruses that encode Bcl-2 homologs. Here we consider the available mechanistic data for viral compared to cellular Bcl-2 protein function along with relevance to the virus life cycle and human disease states.
细胞Bcl-2家族蛋白通过调节线粒体通透性和功能来调控哺乳动物程序性细胞死亡途径中的关键步骤。Bcl-2家族蛋白也由几种大型DNA病毒编码，包括所有已知的γ疱疹病毒、腺病毒和其他几种不相关的病毒。病毒Bcl-2蛋白可以防止细胞死亡，但通常会逃避控制其细胞对应物的细胞调节机制。通过逃避受感染细胞的“利他性”自杀，病毒可以确保在受感染宿主中的复制和传播，但有时方式令人惊讶。许多人类癌症和其他疾病与编码Bcl-2同源物的病毒有关。在这里，我们考虑了与细胞Bcl-2蛋白功能相比，病毒Bcl-2蛋白功能的现有机制数据，以及与病毒生命周期和人类疾病状态的相关性。
