PML B-Box 2 trimerization yields a cysteine triad for arsenic binding in APL therapy
ProMyelocytic Leukemia (PML) protein controls various biological functions, such as apoptosis, senescence or stem cell self-renewal. PML may elicit these functions by scaffolding the spherical shells of PML Nuclear Bodies (NBs), which subsequently act as hubs of post-translational modifications, in particular sumoylation, for the broad range of proteins trafficking through their inner cores. PML NBs are disrupted in Acute Promyelocytic Leukemia (APL) driven by the PML-RARA oncogenic fusion protein.