The Role of PML in Tumor Suppression Paolo Salomoni, Pier Paolo Pandolfi  Cell  Volume 108, Issue 2, Pages 165-170 (January 2002) DOI: 10.1016/S0092-8674(02)00626-8

Figure 1 The PML-NB Modulates p53-Dependent Pathways for Tumor Suppression Oncogenic transformation and DNA damage elicit cellular senescence or induction of apoptosis. These processes are regulated by the tumor suppressor p53. PML controls the targeting of p53 into the PML-NB, its acetylation and transcriptional activation. As a consequence, p53 target genes relevant for either apoptosis or senescence are transcribed. Cell 2002 108, 165-170DOI: (10.1016/S0092-8674(02)00626-8)

Figure 2 The PML-NB Regulates the Assembly and Function of Transcription Factor Complexes Required for Tumor Suppression PML controls the NB-dependent acetylation of p53 by p300/CBP and its transcriptional activation for apoptosis or cellular senescence (left box). The transcription corepressor DAXX is targeted into the PML-NB, from where it modulates DISC-dependent apoptosis (middle box). PML-NB accumulation of an HDAC/N-CoR/Ski-repressing complex is required for MAD and Rb transcription (right box). Cell 2002 108, 165-170DOI: (10.1016/S0092-8674(02)00626-8)