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. Author manuscript; available in PMC: 2013 Jan 2.
Published in final edited form as: FEBS Lett. 2011 Dec 9;586(1):102–106. doi: 10.1016/j.febslet.2011.12.005

Fig. 5. Hypothetical mechanisms for the role of HPV E7 in control of the cellular response to redox-mediated injury and redox-dependent L1 reactivation.

Fig. 5

Redox stress alters both cell signaling and transcription programs. Injury might lead either directly or indirectly to pRb/HDAC-dependent repression of factors required for LINE-1 silencing thus allowing for its reactivation. Cells expressing HPV E7 viral oncoprotein inactivate the Rb/HDAC effect, likely through direct interaction with Rb, thus eliminating the redox-mediated retroelement reactivation.