HPV E6, E6AP and cervical cancer.
HPV E6, E6AP and cervical cancer.
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DOI：
10.1186/1471-2091-9-s1-s4
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发表时间：
2008-10-21
期刊：
影响因子：
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通讯作者：
Huibregtse JM
中科院分区：
文献类型：
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作者：
Beaudenon S;Huibregtse JM
每年约有470,000例新确诊宫颈癌病例，全世界约有230,000名妇女死于这种疾病，其中大多数(约80%)病例和死亡发生在发展中国家。人乳头瘤病毒(HPV)是几乎所有(99.7%)宫颈癌的病原体，而HPVE6蛋白是几乎所有HPV阳性癌症中表达的两种病毒癌蛋白之一。E6劫持了细胞泛素连接酶E6AP，导致P53肿瘤抑制因子以及其他几种细胞蛋白的泛素化和降解。虽然最近针对特定HPV类型的预防性疫苗的引入为预防宫颈癌提供了巨大的希望，但仍然需要治疗方法。E6和E6AP的生化特征已经提出了干扰这些蛋白质的活性的方法，这可能对此目的有用。转载自Current BioData的目标蛋白质数据库(TPdb；)。
Every year, approximately 470,000 new cases of cervical cancer are diagnosed and approximately 230,000 women worldwide die of the disease, with the majority (~80%) of these cases and deaths occurring in developing countries. Human papillomaviruses (HPVs) are the etiological agents in nearly all cases (99.7%) of cervical cancer, and the HPV E6 protein is one of two viral oncoproteins that is expressed in virtually all HPV-positive cancers. E6 hijacks a cellular ubiquitin ligase, E6AP, resulting in the ubiquitylation and degradation of the p53 tumor suppressor, as well as several other cellular proteins. While the recent introduction of prophylactic vaccines against specific HPV types offers great promise for prevention of cervical cancer, there remains a need for therapeutics. Biochemical characterization of E6 and E6AP has suggested approaches for interfering with the activities of these proteins that could be useful for this purpose. Republished from Current BioData's Targeted Proteins database (TPdb; ).