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. 2014 Sep 3;5(19):8879–8892. doi: 10.18632/oncotarget.2432

Figure 6. Dual mechanism of ZMC1.

Figure 6

A1, in the absence of zinc both WT and R175H DBD are in the their zinc free (apo) forms. The Kd1 of WT p53 is << Kd1 of R175H p53 (≈2 nM). The Kd2 of both WT and R175H p53 are ≥ 1 μM. A2, at physiologic concentrations of zinc, WT p53 is zinc bound (holo) (Kd1<[Zn2+]<Kd2). The R175H p53 is in its apo form ([Zn2+]<Kd1<Kd2). A3, in high concentrations of zinc, both WT p53 and R175H p53 are misfolded (Kd1<Kd2<[Zn2+]). A4, in the presence of ZMC1 both WT and R175H p53 are in their holo form despite (Kd1<Kd2<[Zn2+]). B, once the WT conformation change has occurred the increase in ROS by ZMC1 induces N-terminal post-translational modifications of mutant p53 (ser-15, 46, lys-120) that transactivate mutant p53 and induce an apoptotic program.