Oncogenic Human Papillomaviruses (HPVs) base their transforming potential on the action of both
E6 and E7 viral oncoproteins, which perform cooperative or antagonistic actions and thus interfere with a variety of
relevant cellular targets. Among them, the expression of some PDZ-containing polarity proteins, as DLG1 and hScrib,
is altered during the HPV life cycle and the consequent malignant transformation. Together with the well-established
interference of E6 with PDZ proteins, we have recently shown that E7 viral oncoprotein is also responsible for the
changes in abundance and localization of DLG1 observed in HPV-associated lesions. Given that the mechanisms
involved remained only partially understood, we here thoroughly analyse the contribution of a crucial E7 post-translational modifcation: its CKII-dependent phosphorylation. Moreover, we extended our studies to hScrib, in order to
investigate possible conserved regulatory events among diverse PDZ targets of HPV.