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Therefore, multiple viral oncoproteins perturb mitosis through diverse mechanisms leading to an activated DDR.
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Significantly, the DNA-binding domain (DBD) of p73 escapes viral oncoproteins and displays an enhanced thermal stability.
Few reports have documented the transformation of human epithelial cells in the absence of viral oncoproteins [31].
Expression of specific viral oncoproteins, E6 and E7, is required for maintaining the malignant growth of cervical cancer cells [23].
A number of primary human epithelial cells, including esophageal squamous cells, have been transformed using a combination of viral oncoproteins, hTERT, and oncogenic Ras [9], [18], [29], [30].
Mutational analysis has shown that the E6 and E7 viral oncoproteins are necessary and sufficient for the immortalization of human cells by HPV.
Viral oncoproteins can also interact with cellular DNA.
After viral DNA integration in human host-cells, these viral oncoproteins E6 and E7 are overexpressed.
The ability of viral oncoproteins to subvert cell-cycle checkpoints may constitute a mechanism by which viral oncoproteins induce genetic instability (Keating et al, 2001).
The viral oncoproteins E5, E6 and E7 are main players in HPV-associated carcinogenesis.
These findings suggest that key PDZ-containing polarity proteins are common cellular targets of viral oncoproteins.
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