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人乳头瘤病毒E6蛋白的细胞结合伴侣

Cellular binding partners of the human papillomavirus E6 protein.

作者信息

Tungteakkhun Sandy S, Duerksen-Hughes Penelope J

机构信息

Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92354, USA.

出版信息

Arch Virol. 2008;153(3):397-408. doi: 10.1007/s00705-007-0022-5. Epub 2008 Jan 3.

Abstract

The high-risk strains of human papillomavirus (HR-HPV) are known to be causative agents of cervical cancer and have recently also been implicated in cancers of the oropharynx. E6 is a potent oncogene of HR-HPVs, and its role in the progression to malignancy has been and continues to be explored. E6 is known to interact with and subsequently inactivate numerous cellular proteins pivotal in the mediation of apoptosis, transcription of tumor suppressor genes, maintenance of epithelial organization, and control of cell proliferation. Binding of E6 to these proteins cumulatively contributes to the oncogenic potential of HPV. This paper provides an overview of these cellular protein partners of HR-E6, the motifs known to mediate oncoprotein binding, and the agents that have the potential to interfere with E6 expression and activity and thus prevent the subsequent progression to oncogenesis.

摘要

已知人乳头瘤病毒(HR-HPV)的高危毒株是宫颈癌的致病因子,最近也被认为与口咽癌有关。E6是HR-HPV的一种强效癌基因,其在恶性肿瘤进展中的作用一直并仍在被探索。已知E6与许多在细胞凋亡介导、肿瘤抑制基因转录、上皮组织维持和细胞增殖控制中起关键作用的细胞蛋白相互作用,随后使其失活。E6与这些蛋白的结合共同促成了HPV的致癌潜力。本文概述了HR-E6的这些细胞蛋白伙伴、已知介导癌蛋白结合的基序,以及有可能干扰E6表达和活性从而预防随后致癌过程的药物。

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