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-xL, 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-xL 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-xL 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-xL deamidation provides groundings to revisit some concepts related to protein deamidation in general.
Keywords: Aging; Apoptosis; Autophagy; Bcl-x(L); Deamidation; Post-translational modification.
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