Destabilization of the RB tumor suppressor protein and stabilization of p53 contribute to HPV type 16 E7-induced apoptosis
Destabilization of the RB tumor suppressor protein and stabilization of p53 contribute to HPV type 16 E7-induced apoptosis
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DOI：
10.1006/viro.1997.8851
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发表时间：
1997-12-08
期刊：
影响因子：
3.7
通讯作者：
Münger, K
中科院分区：
文献类型：
--
作者：
Jones, DL;Thompson, DA;Münger, K
表达人乳头瘤病毒（HPV） 16型E7癌蛋白的细胞易发生凋亡。以视网膜感光细胞或晶状体细胞为目标表达E7的转基因小鼠在试图进行分化的细胞中表现出凋亡的迹象，我们建立了一个细胞培养系统来研究这一过程，并确定了E7的结构域，该结构域在响应生长停滞信号时易使细胞发生凋亡。E7核心pRB结合位点内的区域是诱导凋亡的必要条件，但不是充分条件。腺病毒保守区1同源结构域内的残基和一致的酪蛋白激酶II磷酸化位点对细胞活力的影响也很重要。我们的数据还表明，E7诱导pRB不稳定和p53稳定的能力与E7介导的转化和凋亡一致，(C) 1997学术出版社。
Cells that express the human papillomavirus (HPV) type 16 E7 oncoprotein are predisposed to undergo apoptosis. Transgenic mice that have E7 expression targeted to either the retinal photoreceptor cells or the lens cells exhibit signs of apoptosis in cells attempting to undergo differentiation, we established a cell culture system to study this process and have determined the domains of E7 that are required for predisposing cells to undergo apoptosis in response to growth arrest signals. Regions within the core pRB binding site of E7 were necessary but not sufficient for inducing apoptosis. Residues within the adenovirus conserved region 1 homology domain and the consensus casein kinase II phosphorylation site are also important for this effect on cell viability. Our data also demonstrate that the ability of E7 to induce destabilization of pRB and stabilization of p53 coincides with E7-mediated transformation and apoptosis, (C) 1997 Academic Press.