HPV E6 oncoprotein prevents recovery of stalled replication forks independently of p53 degradation.

Day T; Vaziri C

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HPV E6 oncoprotein prevents recovery of stalled replication forks independently of p53 degradation.

机译：HPV E6癌蛋白可独立于p53降解而防止停滞的复制叉的恢复。

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The human papillomavirus (HPV) E6 onco-protein hijacks a host cell's E3 ligase, E6AP, altering its substrate specificity to promote p53 polyubiquitylation and proteasome-mediated degradation. Thus, the oncogenic activity of E6 may result in part from destruction of this important tumor suppressor. p53 contributes to maintenance of genome stability in part by enforcing cell cycle checkpoints, yet the role of p53 in mediating S-phase checkpoint responses to DNA-damaging agents is unclear. In a recent report in Cell Cycle, Chen et al. have investi gated the roles of p53 in S-phase checkpoints induced by the ubiquitous environmental agents Benzo(a)pyrene [B(a)P, which generates the DNA-damaging species BPDE] and solar UV radiation [which induces cyclobutane pyrimidine dimers (CPD) and 6-4 photo-products (6-4 PP)].

机译：人乳头瘤病毒（HPV）E6癌蛋白劫持了宿主细胞的E3连接酶E6AP，从而改变了其底物特异性，从而促进了p53多泛素化和蛋白酶体介导的降解。因此，E6的致癌活性可能部分是由于这种重要的肿瘤抑制剂的破坏所致。 p53部分地通过执行细胞周期检查点来维持基因组稳定性，但是p53在介导S期检查点对DNA破坏剂的反应中的作用尚不清楚。在《细胞周期》的最新报告中，Chen等人。已经研究了p53在普遍存在的环境因子苯并（a）re [B（a）P，它会产生破坏DNA的物种BPDE]和太阳紫外线辐射[诱导环丁烷嘧啶二聚体（ CPD）和6-4照片产品（6-4 PP）]。

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《Cell cycle》 |2009年第14期|共1页
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Day T; Vaziri C;
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中图分类细胞生物学;
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1. HPV E6 oncoprotein prevents recovery of stalled replication forks independently of p53 degradation. [J] . Day T, Vaziri C Cell cycle . 2009,第14期

机译：HPV E6癌蛋白可独立于p53降解而防止停滞的复制叉的恢复。
2. HPV-16 E6 oncoprotein impairs the fidelity of DNA end-joining via p53-dependent and -independent pathways [J] . Ki-Hyuk Shin, Jae Hoon Ahn, Mo K. Kang, International journal of oncology . 2006,第1期

机译：HPV-16 E6癌蛋白通过P53依赖性和依赖性途径损害DNA终端连接的保真度
3. p53 prevents the accumulation of double-strand DNA breaks at stalled-replication forks induced by UV in human cells. [J] . Squires S, Coates JA, Goldberg M, Cell cycle . 2004,第12期

机译：p53阻止了紫外线在人细胞中在停滞的复制叉处积累双链DNA断裂。
4. FRAGMENT-BASED DESIGN OF NOVEL INHIBITORS OF HPV 16 E6 ONCOPROTEIN:MOLECULAR DOCKING,MOLECULAR DYNAMICS SIMULATION AND IN SILICO ADME ANALYSIS [C] . A.Kumar, E.Rathi, S.G.Kini Conference on Drug Design and Discovery Technologies . 2020

机译：基于片段的HPV 16 E6癌蛋白的新型抑制剂设计：分子对接，分子动力学模拟和硅Adme分析
5. A chemical genetic screen to identify small molecule inhibitors of HPV E6-mediated p53 degradation. [D] . Liou, Kwa Yu. 2007

机译：化学遗传筛选，以鉴定HPV E6介导的p53降解的小分子抑制剂。
6. HPV E6 Oncoprotein Prevents Recovery of Stalled Replication Forks Independently of p53 Degradation [O] . Tovah Day, Cyrus Vaziri -1

机译：复制叉停滞的HpV E6癌蛋白可以防止恢复独立的p53降解
7. ATR and ATM differently regulate WRN to prevent DSBs at stalled replication forks and promote replication fork recovery [O] . Ammazzalorso, Francesca, Pirzio, Livia Maria, Bignami, Margherita, 2010

机译：ATR和ATM对WRN的管理方式有所不同，以防止DSB停滞在复制叉中并促进复制叉恢复

HPV E6 oncoprotein prevents recovery of stalled replication forks independently of p53 degradation.

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