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Human papilloma virus (HPV) is present in greater than 90 percent of cervical cancers. HPV encodes two proteins, E6 and E7, that are potent contributors to its tumorigenicity. E7 is known to disable RB; E6 binds to p53 and targets it for degradation. How will this affect apoptosis?

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Final answer:

HPV's E6 protein binds to and leads to the degradation of the tumor suppressor protein p53, preventing apoptosis and allowing potentially cancerous cells to divide unchecked.

Step-by-step explanation:

When the human papillomavirus (HPV) infects a cell, it produces the E6 protein, which binds to the p53 protein. Normally, p53 acts as a tumor suppressor by triggering apoptosis in cells with damaged DNA, thereby preventing the cells from becoming cancerous. However, when E6 binds to p53, it leads to the inactivation and degradation of p53. Consequently, this prevents apoptosis, allowing cells with mutations to survive and proliferate unchecked, increasing the risk of cancer development, particularly cervical cancer. The most likely effect of E6 binding on p53 activity, therefore, is that it marks p53 for degradation, which impairs the normal function of p53 in apoptosis and cell cycle regulation.

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