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Human papillomavirus E6 and E7 oncoproteins as risk factors for tumorigenesis. Review 133 refs

机译:人瘤病毒 E6 和 E7 癌蛋白作为肿瘤发生的危险因素。评论133 参考文献

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Human papillomavirus (HPV) is small, double-stranded DNA virus that infects mucosal and cutaneous epithelial tissue. HPV is sexually transmitted and the viral DNA replicates extrachromosomally. The virus is non-enveloped and has an icosahedral capsid. There are approximately 118 types of HPV, which are characterized as high-risk or low- risk types. High-risk HPVs cause malignant transformation while the low-risk ones cause benign warts and lesions. The expression of E6 and E7 is normally controlled during the normal viral life cycle when viral DNA replicates extrachromosomally. HPV E6 and E7 oncoproteins are overexpressed when the viral genome integrates into the host DNA.Deregulated overexpression of E6 and E7 oncoproteins can cause several changes in cellular pathways and functions leading to malignant transformation of cells and tumorigenesis. In this review, we focus on several cellular mechanisms and pathways that are altered in the presence of E6 and E7, the target proteins of E6 and E7 inside the host cell and how they contribute to the development of the transformed phenotype. References: 133
机译:人瘤病毒 (HPV) 是一种感染粘膜和皮肤上皮组织的小型双链 DNA 病毒。HPV通过性传播,病毒DNA在染色体外复制。该病毒是无包膜的,具有二十面体衣壳。HPV大约有118种类型,分为高风险或低风险类型。高危型HPV会引起恶性转化,而低危型HPV会引起良性疣和病变。当病毒 DNA 在染色体外复制时,E6 和 E7 的表达通常在正常的病毒生命周期内受到控制。当病毒基因组整合到宿主 DNA 中时,HPV E6 和 E7 癌蛋白会过表达。E6 和 E7 癌蛋白的失调过表达可引起细胞通路和功能的多种变化,导致细胞恶性转化和肿瘤发生。在这篇综述中,我们重点关注在宿主细胞内E6和E7的靶蛋白E6和E7存在下改变的几种细胞机制和途径,以及它们如何促进转化表型的发展。[参考资料:133]

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