Bcl-xL deamidation and cancer: Charting the fame trajectories of legitimate child and hidden siblings

Bcl-2 family proteins control programmed cell death through a complex network of interactions within and outside of this family, that are modulated by post-translational modifications (PTM). Bcl-x(L), an anti-apoptotic member of this family, is overexpressed in a number of cancers, plays an important role in tumorigenesis and is correlated with drug resistance. Bcl-x(L) is susceptible to a number of different PTMs. Here, we focus on deamidation. We will first provide an overview of protein deamidation. We will then review how the apoptotic and autophagic functions of Bcl-x(L) are modified by this PTM, and how this impacts on its oncogenic properties. Possible therapeutic outcomes will also be discussed. Finally, we will highlight how the specific case of Bcl-x(L), deamidation provides groundings to revisit some concepts related to protein deamidation in general.