p53介导的具有复制型乙型肝炎病毒的细胞对DNA损伤的细胞反应。
p53-mediated cellular response to DNA damage in cells with replicative hepatitis B virus.
作者信息
Puisieux A, Ji J, Guillot C, Legros Y, Soussi T, Isselbacher K, Ozturk M
机构信息
Laboratoire d'Oncologie Moléculaire, Institut National de la Santé et de la Recherche Médicale CJF 9302, Centre Léon Bérard, Lyon, France.
出版信息
Proc Natl Acad Sci U S A. 1995 Feb 28;92(5):1342-6. doi: 10.1073/pnas.92.5.1342.
Wild-type p53 acts as a tumor suppressor gene by protecting cells from deleterious effects of genotoxic agents through the induction of a G1/S arrest or apoptosis as a response to DNA damage. Transforming proteins of several oncogenic DNA viruses inactivate tumor suppressor activity of p53 by blocking this cellular response. To test whether hepatitis B virus displays a similar effect, we studied the p53-mediated cellular response to DNA damage in 2215 hepatoma cells with replicative hepatitis B virus. We demonstrate that hepatitis B virus replication does not interfere with known cellular functions of p53 protein.
野生型p53作为一种肿瘤抑制基因，通过诱导G1/S期阻滞或凋亡来保护细胞免受基因毒性剂的有害影响，从而对DNA损伤作出反应。几种致癌DNA病毒的转化蛋白通过阻断这种细胞反应来使p53的肿瘤抑制活性失活。为了测试乙型肝炎病毒是否具有类似作用，我们研究了具有复制性乙型肝炎病毒的2215肝癌细胞中p53介导的对DNA损伤的细胞反应。我们证明乙型肝炎病毒复制不会干扰p53蛋白已知的细胞功能。
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