Journal
VIRUSES-BASEL
Volume 13, Issue 8, Pages -Publisher
MDPI
DOI: 10.3390/v13081662
Keywords
HPV; skin cancer; p300; DNA damage; proliferation; differentiation; UV
Categories
Funding
- Terry Johnson Basic Cancer Research Center
- United States' Department of Defense's Congressionally Directed Medical Research Program's Peer Reviewed Cancer Research Program [CMDRP PRCRP CA160224]
- National Institutes of Health [NCI R15 CA242057 01A1]
- National Institute of General Medical Sciences (NIGMS) of the National Institutes of Health [P20GM130448]
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This review focuses on HPV8 from the beta genus of human papillomaviruses, which counteracts the cellular response to damaged DNA and mitotic errors by destabilizing a histone acetyltransferase, p300, leading to broad dysregulation of cell signaling and decreased genome stability. Moreover, it discusses the extent to which E6 from other beta-HPVs destabilizes p300 and dissecting HPV8 E6 biology using mutants.
The beta genus of human papillomaviruses infects cutaneous keratinocytes. Their replication depends on actively proliferating cells and, thus, they conflict with the cellular response to the DNA damage frequently encountered by these cells. This review focus on one of these viruses (HPV8) that counters the cellular response to damaged DNA and mitotic errors by expressing a protein (HPV8 E6) that destabilizes a histone acetyltransferase, p300. The loss of p300 results in broad dysregulation of cell signaling that decreases genome stability. In addition to discussing phenotypes caused by p300 destabilization, the review contains a discussion of the extent to which E6 from other beta-HPVs destabilizes p300, and provides a discussion on dissecting HPV8 E6 biology using mutants.
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