This result indicates that enhanced NEDDylation increases cell sensitivity to H2O2 treatment.
Increased miR-181a expression in mature T-cells augments cell sensitivity to peptide antigens.
Cell sensitivity to drug treatments was assessed using colony forming assays.
The most effective molecular target which was correlated with TMZ cell sensitivity was Lig4.
Moreover, Ubc12 knockout decreases cell sensitivity to H2O2-induced oxidative stress, but NEDP1 deletion aggravates this sensitivity.
Open image in new window Figure 7 NEDDylation regulates cell sensitivity to H 2 O 2 -induced oxidative stress.
The cell sensitivity to the PEF seems to be affected by the cell diameter.
However, since the groups used different cell models, cell uptake and cell sensitivity may well play an important role.
Conversely, activation of caspase-3 often increases cancer cell sensitivity to apoptosis (Devarajan et al., 2002; Guicciardi and Gores, 2013).
Moreover, NEDP1 deletion reduced PCNA-polη interaction, thus prevented TLS pathway and increased cell sensitivity to H2O2-induced oxidative stress (Figs. 6B and 7A).
While in Ubc12 −/− cells, we found that UBC12 deletion increased cell survival while UBC12 re-expression increased cell sensitivity to oxidative stress induced by H2O2 treatment (Fig. 7B).
