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Production of viral progeny is coordinated by the action of the HPV oncoproteins E6 and E7 which modulate cell growth and differentiation, the replication and transcription factors E1 and E2, and the structural proteins L1 and L2. Cellular immortalization by HPVs is restricted to the high-risk types and is induced by the association of E6 and E7 with cellular proteins that regulate cell growth. The interactions of E7 with the retinoblastoma tumor suppressor protein (p105Rb) and E6 with the tumor suppressor p53 play central roles in these processes [4].

Sparkowski J, Mense M, Anders J, Schlegel R: E5 oncoprotein transmembrane mutants dissociate fibroblast transforming activity from 16-kilodalton protein binding and platelet-derived growth factor receptor binding and phosphorylation. J Virol 1996;70:2420–2430. Suprynowicz FA, Sparkowski J, Baege A, Schlegel R: E5 oncoprotein mutants activate phosphoinositide 3-kinase independently of platelet-derived growth factor receptor activation. J Biol Chem 2000;275:5111–5119. Ghai J, Ostrow RS, Tolar J, McGlennen RC, Lemke TD, Tobolt D, Liu Z, Faras AJ: The E5 gene product of rhesus papillomavirus is an activator of endogenous Ras and phosphatidylinositol3Ј-kinase in NIH 3T3 cells.

Proc Natl Acad Sci USA 1987;84:3695–3698. Sock E, Wegner M, Grummt F: DNA replication of human polyomavirus JC is stimulated by NF-1 in vivo. Virology 1991;182:298–308. Cheng L, Kelly TJ: Transcriptional activator nuclear factor 1 stimulates the replication of SV40 minichromosomes in vivo and in vitro. Cell 1989;59:541–551. Miyamura T, Furuno A, Yoshiike K: DNA rearrangement in the control region for early transcription in a human polyomavirus JC host range mutant capable of growing in human embryonic kidney cells.

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A histone H3K36 chromatin switch coordinates DNA double-strand break repair pathway choice

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