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Journal of Virology, November 2007, p. 12675-12679, Vol. 81, No. 22
0022-538X/07/$08.00+0 doi:10.1128/JVI.01083-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Department of Pathology, University of Virginia School of Medicine, Charlottesville, Virginia
Received 19 May 2007/ Accepted 27 August 2007
The attachment and spreading of keratinocyte cells result from interactions between integrins and immobilized extracellular matrix molecules. Human papillomavirus type 16 (HPV-16) E6 augmented the kinetics of cell spreading, while E6 genes from HPV-11 or bovine papillomavirus type 1 did not. The ability of E6 to interact with the E6AP ubiquitin ligase and target p53 degradation was required to augment cell-spreading kinetics; dominant negative p53 alleles also enhanced the kinetics of cell spreading and the level of attachment of cells to hydrophobic surfaces. The targeted degradation of p53 by E6 may contribute to the invasive phenotype exhibited by cervical cells that contain high-risk HPV types.
Published ahead of print on 5 September 2007.
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