乳头瘤病毒E6的PDZ相互作用可被p53的抑制所取代，以促进游离型人乳头瘤病毒基因组的维持。
Papillomavirus E6 PDZ interactions can be replaced by repression of p53 to promote episomal human papillomavirus genome maintenance.
作者信息
Brimer Nicole, Vande Pol Scott B
机构信息
Department of Pathology, University of Virginia, Charlottesville, Virginia, USA.
出版信息
J Virol. 2014 Mar;88(5):3027-30. doi: 10.1128/JVI.02360-13. Epub 2013 Dec 18.
Abstract
Cancer-associated human papillomaviruses (HPVs) express E6 oncoproteins that target the degradation of p53 and have a carboxy-terminal PDZ ligand that is required for stable episomal maintenance of the HPV genome. We find that the E6 PDZ ligand can be deleted and the HPV genome stably maintained if cellular p53 is inactivated. This indicates that the E6-PDZ interaction promotes HPV genome maintenance at least in part by neutralization of an activity that can arise from residual undegraded p53.
摘要
与癌症相关的人乳头瘤病毒（HPV）表达E6癌蛋白，该蛋白靶向p53的降解，并且具有一个羧基末端PDZ配体，这是HPV基因组稳定游离维持所必需的。我们发现，如果细胞中的p53失活，E6 PDZ配体可以被删除，并且HPV基因组能够稳定维持。这表明E6-PDZ相互作用至少部分地通过中和由残留未降解的p53产生的活性来促进HPV基因组的维持。
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