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N-alpha-acetyltransferase 10, NatA catalytic subunit (NAA10), is the catalytic component of the NatA N-terminal acetyltransferase complex, responsible for the highly prevalent modification of N-terminal protein acetylation in eukaryotic cells[1][3]. NAA10 transfers an acetyl group from acetyl-CoA to the alpha-amino group at the N-terminus of nascent polypeptides, especially after methionine excision, affecting nearly 40–50% of the proteome[1][2][3]. NAA10 influences protein stability, subcellular localization, and interaction networks and has broad roles in cellular processes including cell cycle, DNA repair, migration, apoptosis, and transcription regulation[1][2]. Defects or mutations in NAA10 are linked to developmental disorders (notably Ogden syndrome and syndromic microphthalmia) and play a role in cancer biology, sometimes by suppressing tumor growth or metastasis[3]. Some recently developed bisubstrate inhibitors target NAA10, supporting its consideration as a pharmacological target, but its essential cellular functions also introduce potential safety risks when targeting this enzyme[2][3].
Inhibitors: Block the catalytic activity of NAA10, preventing N-terminal acetylation of substrate proteins[2].
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