Neural Regeneration Research ›› 2025, Vol. 20 ›› Issue (10): 2862-2871.doi: 10.4103/NRR.NRR-D-24-00779

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Exploring the role of N-acetyltransferases in diseases: a focus on N-acetyltransferase 9 in neurodegeneration

Prajakta Deshpande1, #, Anuradha Venkatakrishnan Chimata1, #, Amit Singh1, 2, 3, 4, 5, *   

  1. 1 Department of Biology, University of Dayton, Dayton, OH, USA;  2 Premedical Program, University of Dayton, Dayton, OH, USA;  3 Center for Tissue Regeneration and Engineering at Dayton (TREND), University of Dayton, Dayton, OH, USA;  4 Integrative Science and Engineering Center, University of Dayton, Dayton, OH, USA;  5 Center for Genomic Advocacy (TCGA), Indiana State University, Terre Haute, IN, USA
  • Online:2025-10-15 Published:2025-02-07
  • Contact: Amit Singh, PhD, asingh1@udayton.edu.
  • Supported by:
    This work was supported by 1RO1EY032959-01 and RO1 supplement from NIH, Schuellein Chair Endowment Fund and STEM Catalyst Grant from the University of Dayton (to AS).

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Abstract: Acetyltransferases, required to transfer an acetyl group on protein are highly conserved proteins that play a crucial role in development and disease. Protein acetylation is a common post-translational modification pivotal to basic cellular processes. Close to 80%– 90% of proteins are acetylated during translation, which is an irreversible process that affects protein structure, function, life, and localization. In this review, we have discussed the various N-acetyltransferases present in humans, their function, and how they might play a role in diseases. Furthermore, we have focused on N-acetyltransferase 9 and its role in microtubule stability. We have shed light on how N-acetyltransferase 9 and acetylation of proteins can potentially play a role in neurodegenerative diseases. We have specifically discussed the N-acetyltransferase 9-acetylation independent function and regulation of c-Jun N-terminal kinase signaling and microtubule stability during development and neurodegeneration.

Key words: acetyl-coenzyme A, Alzheimer’s disease, animal models, cell death, drosophila, eye, human disease, c-Jun N-terminal kinase signaling, N-Acetyltransferases, N-acetyltransferase 9, neurodegeneration