RESUMO
Protein N-terminal (Nt) acetylation is an essential post-translational process catalysed by N-acetyltransferases or N-terminal acetyltransferases (NATs). Over the past several decades, several types of NATs (NatA- NatH) have been identified along with their substrates, explaining their significance in eukaryotes. It affects protein stability, protein degradation, protein translocation, and protein-protein interaction. NATs have recently drawn attention as they are associated with the pathogenesis of human diseases. In particular, NAT-induced epigenetic modifications play an important role in the control of mitochondrial function, which may lead to inflammatory diseases. NatC knockdown causes a marked reduction in mitochondrial membrane proteins, impairing their functions, and NatA affects mitophagy via reduced phosphorylation and transcription of the autophagy receptor. However, the NAT-mediated mitochondrial epigenetic mechanisms involved in the inflammatory process remain unexplored. The current review will impart an overview of the biological functions and aberrations of various NAT, which may provide a novel therapeutic strategy for inflammatory disorders.
