NAT1 (N-acetyltransferase 1) is a phase II drug-metabolizing enzyme belonging to the arylamine N-acetyltransferase family. It catalyzes the transfer of an acetyl group from acetyl-CoA to aromatic amines, hydrazines, and heterocyclic amines, facilitating the detoxification or bioactivation of xenobiotics, including environmental carcinogens (e.g., tobacco smoke components) and certain pharmaceuticals. Unlike its isoform NAT2. which is predominantly expressed in the liver and associated with genetic polymorphisms affecting drug metabolism, NAT1 exhibits broader tissue distribution, including the gut, lungs, and kidneys, and is implicated in both metabolic and non-metabolic roles.
NAT1 has garnered attention for its potential links to cancer. Genetic variations or altered expression of NAT1 may influence susceptibility to malignancies such as breast, colorectal, and bladder cancers, possibly through dysregulation of folate metabolism or interactions with oncogenic pathways. Recent studies also suggest NAT1’s involvement in cellular processes like proliferation and apoptosis, independent of its enzymatic activity.
NAT1 antibodies are essential tools for investigating its expression patterns, localization, and functional roles in disease models. They are widely used in techniques like Western blotting, immunohistochemistry, and immunofluorescence to assess NAT1 levels in normal vs. tumor tissues or to study its regulation under pharmacological or pathological conditions. Additionally, these antibodies aid in exploring NAT1 as a therapeutic target or biomarker, particularly in cancers where its overexpression correlates with prognosis. Research continues to unravel its complex biology, bridging gaps between acetylation genetics, environmental exposures, and disease mechanisms.