1995/01/01 by Sandy S. Tungteakkhun, Penelope J. Duerksen-Hughes, Miguel Díaz-Pache Pumareda
Biochemistry, Genetics and Molecular Biology · Business, Management and Accounting · Computer Science · Engineering · Immunology and Microbiology · Medicine · #Cervical Cancer and HPV Research #Distributed systems and fault tolerance #Law, Ethics, and AI Impact #NF-κB Signaling Pathways #Space Exploration and Technology #interferon and immune responses
paper · pdf · doi:10.1007/s00705-007-0022-5
openalex publication_date 1995/01/01 · openalex created_date 2016/06/24 · openalex updated_date 2026/07/31
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.