Finally, Xia et al. showed that Wip1 not only protects from DNA damage-induced apoptosis, but also protects the cell from apoptosis induced by various types of oxidative and ribotoxic stress (72). Wip1−/− MEFs exhibited higher levels of apoptosis (as measured by flow cytometry, nuclei morphology, and Caspase and PARP cleavage) after treatment with anisomycin, etoposide, H202, UV radiation, or staurosporine. Furthermore, Wip1−/− MEFs have higher levels of active p38 MAPK and JNK/c-jun pathways. Therefore, the authors concluded that Wip1 is a global regulator of apoptosis through the inhibition of p38 MAPK, JNK, and c-jun pathways (72).
