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Fig. 1 | BMC Cancer

Fig. 1

From: Novel effect of the high risk-HPV E7 CKII phospho-acceptor site on polarity protein expression

Fig. 1

Mutation of the HPV-18 E7 CKII phospho-acceptor site prevents the stabilization of DLG1. A C4-1 wild type cells and the CKII HPV-18 E7 phospho-acceptor mutant derivative (C4-1 B8 and C4-1 A15) cells were grown for 24 h and whole protein extracts were analysed by Western Blot (Left panel). The endogenous expression of DLG1 was ascertained using the specific anti-DLG1 antibody. α-tubulin was used as loading control. Right panel, densitometry analysis of western blots for DLG1 expression, normalised for α-tubulin levels in each corresponding different condition (mean ± SD, n = 3). Asterisks denote significant differences determined by ANOVA test (**p < 0.05). B HEK293 epithelial cells were transiently transfected with 5 µg of pseyfp2-18 E6, 5 µg of wild type or 5 µg of mutant pCMV-Flag-18 E7 and 1 µg of pmTurq2-DLG1 plasmid. Cells were harvested 24 h post-transfection and the expression of fusion proteins was assessed by Western Blot (Left panel) using an anti-Flag (wild type and mutant 18E7), anti-18E6 and anti-GFP, which recognizes mTurq2-DLG1. β-Galactoside levels were used as transfection control. For the assessment of the E7-Flag proteins two images with different degree of exposition are shown for a better appreciation. Right panel, densitometry analysis of western blots for DLG1 expression for equal β-galactoside levels in each corresponding different condition (mean ± SD, n = 3). Asterisks denote significant difference determined by ANOVA test and a Multiple Comparisons Tukey´s test (***p < 0.005, ****p < 0.0005) and “ns” indicates no significant changes. Original blots are presented in the Fig. S3 and Fig. S4

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