Human Papillomavirus Type 16 L2 DNA Methylation in Exfoliated Cervical Cells From College-Age Women

2017 ◽  
Vol 21 (2) ◽  
pp. 162
2016 ◽  
Vol 20 (4) ◽  
pp. 332-337 ◽  
Author(s):  
Erin L. Anderson ◽  
Carolyn E. Banister ◽  
Susannah Kassler ◽  
Amy Messersmith ◽  
Lucia Pirisi ◽  
...  

Virology ◽  
2009 ◽  
Vol 389 (1-2) ◽  
pp. 100-107 ◽  
Author(s):  
Janet L. Brandsma ◽  
Ying Sun ◽  
Paul M. Lizardi ◽  
David P. Tuck ◽  
Daniel Zelterman ◽  
...  

2014 ◽  
Vol 59 (1) ◽  
pp. 24-29 ◽  
Author(s):  
Dean Bryant ◽  
Amanda Tristram ◽  
Triantafillos Liloglou ◽  
Samantha Hibbitts ◽  
Alison Fiander ◽  
...  

1995 ◽  
Vol 71 (2) ◽  
pp. 246-249 ◽  
Author(s):  
AM Simons ◽  
C Múgica van Herckenrode ◽  
JA Rodriguez ◽  
N Maitland ◽  
M Anderson ◽  
...  

Virology ◽  
2011 ◽  
Vol 412 (1) ◽  
pp. 146-155 ◽  
Author(s):  
Christine Weyn ◽  
Jean-Marie Vanderwinden ◽  
Joanne Rasschaert ◽  
Yvon Englert ◽  
Véronique Fontaine

2007 ◽  
Vol 81 (22) ◽  
pp. 12675-12679 ◽  
Author(s):  
Brooke Cooper ◽  
Nicole Brimer ◽  
Scott B. Vande Pol

ABSTRACT 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.


2009 ◽  
Vol 13 (2) ◽  
pp. 212-219 ◽  
Author(s):  
Peechanika Chopjitt ◽  
Tipaya Ekalaksananan ◽  
Chamsai Pientong ◽  
Bunkerd Kongyingyoes ◽  
Pilaiwan Kleebkaow ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document