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. Author manuscript; available in PMC: 2008 Feb 2.
Published in final edited form as: Int J Cancer. 2006 Oct 15;119(8):1878–1885. doi: 10.1002/ijc.22064

Figure 3.

Figure 3

E6 retains its ability to activate the hTERT promoter when an E-box mutated, myc-unresponsive construct (TERT-E-luc) or X-box mutated construct are used. (a) E-box and X-box mutants contain transversion mutations at conserved binding sequences in the promoter. (b) Luciferase assays were performed with transiently transfected wild-type TERT-luc or mutant TERT-E-luc constructs in triplicate. Error bars represent 1 standard deviation from the mean. Activation of the hTERT promoter by a c-Myc expression construct is abolished with the E-box mutation. (c) HFKs were transfected with pGL3-basic, TERT-luc, TERT-E-luc or TERT-X luciferase reporter vectors respectively. Activation of the promoter constructs by E6 when compared to non-E6 expressing vector controls is expressed as percentage of full activation of the wild-type promoter by E6. Approximately 65% activation by E6 is retained when the E-box is mutated. Mutation of the X-box element of the hTERT promoter (TERT X-luc) results in no significant decrease in activation by E6. Where not indicated, E6E7 expressing HFKs are at early passage. Experiments were performed in triplicate. Error bars represent 1 standard deviation from the mean.