Oleksi Petrenko

TL;DR: Evidence that p53 translocation to the mitochondria occurs in vivo in irradiated thymocytes is provided and it is shown that the p53 protein can directly induce permeabilization of the outer mitochondrial membrane by forming complexes with the protective BclXL and Bcl2 proteins, resulting in cytochrome c release.

TL;DR: Because the p53-MDM2 interaction is structurally and biologically well understood, the design of small lipophilic molecules that disrupt or prevent it has become an important target for cancer therapy.

TL;DR: The results suggest that in sensitive organs mitochondrial p53 accumulation in vivo occurs soon after a death stimulus, triggering a rapid first wave of apoptosis that is transcription independent and may precede a second slower wave that are transcription dependent.

TL;DR: The data provide direct genetic evidence for a functional link between MIF and the p53 tumor suppressor and indicate an important and previously unappreciated role for MIF in carcinogenesis.

TL;DR: It is reported here that ΔNp73 confers resistance to spontaneous replicative senescence of primary mouse embryo fibroblasts (MEFs) and immortalizes MEFs at a 1,000-fold-higher frequency than occurs spontaneously and behaves as an oncogene that targets p53 that might explain why ΔN p73 upregulation may be selected for during tumorigenesis of human cancers.