Role of the post-translational modifications of HSP60 in disease

Abstract

Heat Shock Protein 60 (HSP60) is primarily a chaperone protein responsible for refolding proteins in the mitochondria. Nevertheless it has numerous other pro- and anti-apoptotis and signalling functions which it achieves through a variety of post-translational modifications (PTMs). Increasing evidence indicates that in disease states from cancer to systemic inflammation, such modifications become dysregulated, and as a result HSP60 cannot perform its functions. Understanding the biological role of these PTMs in healthy and disease states, the context in which they are generated and removed, as well as the mechanisms by which they can be targetted and modulated extraneously will help to provide better therapeutic solutions to deal with a wide range of conditions driven by stress-related processes.