Inactivation of the CYLD deubiquitinase by HPV E6 mediates hypoxia-induced NF-kappaB activation.

An J; Mo D; Liu H; Veena MS; Srivatsan ES; Massoumi R; Rettig MB

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Inactivation of the CYLD deubiquitinase by HPV E6 mediates hypoxia-induced NF-kappaB activation.

机译：HPV E6对CYLD去泛素酶的灭活介导了缺氧诱导的NF-κB活化。

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The biochemical mechanisms that underlie hypoxia-induced NF-kappaB activity have remained largely undefined. Here, we find that prolonged hypoxia-induced NF-kappaB activation is restricted to cancer cell lines infected with high-risk human papillomavirus (HPV) serotypes. The HPV-encoded E6 protein is necessary and sufficient for prolonged hypoxia-induced NF-kappaB activation in these systems. The molecular target of E6 in the NF-kappaB pathway is the CYLD lysine 63 (K63) deubiquitinase, a negative regulator of the NF-kappaB pathway. Specifically, hypoxia stimulates E6-mediated ubiquitination and proteasomal degradation of CYLD. Given the established role of NF-kappaB in human carcinogenesis, these findings provide a potential molecular/viral link between hypoxia and the adverse clinical outcomes observed in HPV-associated malignancies.

机译：缺氧诱导的NF-κB活性基础的生化机制仍未明确。在这里，我们发现长时间缺氧诱导的NF-κB活化仅限于感染高危人乳头瘤病毒（HPV）血清型的癌细胞系。 HPV编码的E6蛋白对于在这些系统中长时间缺氧诱导的NF-κB激活是必要的和充分的。 NF-kappaB途径中E6的分子靶标是CYLD赖氨酸63（K63）去泛素酶，它是NF-kappaB途径的负调节剂。具体而言，缺氧会刺激E6介导的泛素化和CYLD的蛋白酶体降解。鉴于NF-κB在人类致癌作用中已确立的作用，这些发现为缺氧与HPV相关性恶性肿瘤的不良临床结果之间提供了潜在的分子/病毒联系。

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《Cancer Cell》 |2008年第5期|共14页
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An J; Mo D; Liu H; Veena MS; Srivatsan ES; Massoumi R; Rettig MB;
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正文语种 eng
中图分类肿瘤学;
关键词
Animals; Cell Adhesion; Cell Hypoxia; Cells; Cultured; Electrophoretic Mobility Shift Assay; 动物; 细胞粘附; 细胞低氧; 细胞; 培养的; 表皮; 角蛋白细胞; 小鼠; 小鼠; 裸;

机译：Animals;Cell Adhesion;Cell Hypoxia;Cells;Cultured;Electrophoretic Mobility Shift Assay;动物;细胞粘附;细胞低氧;细胞;培养的;表皮;角蛋白细胞;小鼠;小鼠;裸;

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1. Inactivation of the CYLD deubiquitinase by HPV E6 mediates hypoxia-induced NF-kappaB activation. [J] . An J, Mo D, Liu H, Cancer Cell . 2008,第5期

机译：HPV E6对CYLD去泛素酶的灭活介导了缺氧诱导的NF-κB活化。
2. CYLD, a deubiquitinase specific for lysine63-linked polyubiquitins, accumulates at the postsynaptic density in an activity-dependent manner [J] . DosemeciA., TheinS., YangY., Biochemical and Biophysical Research Communications . 2013,第1期

机译：CYLD是一种特异性针对赖氨酸63连接的多聚泛素的去泛素酶，其以依赖于活性的方式在突触后密度积累
3. Inactivation of deubiquitinase CYLD enhances therapeutic antibody production in Chinese hamster ovary cells [J] . Lu Yafang, Zhou Qin, Han Qianqian, Applied Microbiology and Biotechnology . 2018,第14期

机译：脱硫蛋白酶的失活增强了中国仓鼠卵巢细胞中的治疗性抗体生产
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 novel mechanism for human papillomavirus mediated tumorigenesis: Examining a role for HPV E6 protein in CYLD mediated NF-kappaB activation. [D] . Shaw, Charlie Vincent, Jr. 2009

机译：人类乳头瘤病毒介导的肿瘤发生的新机制：检查HPV E6蛋白在CYLD介导的NF-κB激活中的作用。
6. Inactivation of the CYLD Deubiquitinase by HPV E6 Mediates Hypoxia-Induced NF-κB Activation [O] . Jiabin An, Deqiong Mo, Huiren Liu, -1

机译：HPV E6对CYLD去泛素酶的失活介导了缺氧诱导的NF-κB激活。
7. Inactivation of the CYLD Deubiquitinase by HPV E6 Mediates Hypoxia-Induced NF-κB Activation [O] . An Jiabin, Mo Deqiong, Liu Huiren, 2008

机译：HPV E6对CYLD去泛素酶的失活介导了缺氧诱导的NF-κB激活。

Inactivation of the CYLD deubiquitinase by HPV E6 mediates hypoxia-induced NF-kappaB activation.

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