Abstract
Human papillomavirus (HPV) E7 is essential in inducing S-phase progression in differentiating epithelial cells. We have previously shown that HPV-16 E7 activity can be controlled by a direct interaction with the viral transcriptional activator E2, thereby inhibiting transforming potential of E7. We have extended these analyses to show that E2 induces a generalized re-localization of E7 within the cell nucleus, one potential consequence of which is the inhibition of E7-induced degradation of pRb. Most importantly, we show that E2 can also inhibit the ability of E7 to induce centrosome abnormalities, thus preventing aberrant mitoses. Taken together, these studies highlight the central importance of E2 in controlling the functions of E7, independently of the ability of E2 to regulate transcription.
Original language | English |
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Pages (from-to) | 2299-304 |
Number of pages | 6 |
Journal | Oncogene |
Volume | 28 |
Issue number | 23 |
DOIs | |
Publication status | Published - 11 Jun 2009 |
Keywords / Materials (for Non-textual outputs)
- Blotting, Western
- Cell Line, Tumor
- Cell Nucleus
- Centrosome
- DNA-Binding Proteins
- Fluorescent Antibody Technique
- Gene Expression Regulation, Viral
- Humans
- Oncogene Proteins, Viral
- Papillomavirus E7 Proteins
- Plasmids
- Protein Binding
- Retinoblastoma Protein
- Reverse Transcriptase Polymerase Chain Reaction
- Transfection