TY - JOUR
T1 - Cellular binding partners of the human papillomavirus E6 protein
AU - Tungteakkhun, Sandy S.
AU - Duerksen-Hughes, Penelope J.
N1 - Funding Information:
I would like to acknowledge my NIH grant: R01 CA095461 from the National Cancer Institute.
PY - 2008/3
Y1 - 2008/3
N2 - 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.
AB - 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.
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U2 - 10.1007/s00705-007-0022-5
DO - 10.1007/s00705-007-0022-5
M3 - Short survey
C2 - 18172569
SN - 0304-8608
VL - 153
SP - 397
EP - 408
JO - Archives of Virology
JF - Archives of Virology
IS - 3
ER -