N-Acetyl-L-alanine

N-Acetyl-L-alanine is an endogenous metabolite.^1,2,3 It decreases IFN-γ production induced by radiation-killed M. tuberculosis in natural killer (NK) cells isolated from patients with latent M. tuberculosis infection when used at a concentration of 3 µM.¹ N-Acetyl-L-alanine (3 µM) also decreases ATP production and glycolytic flux in naïve or radiation-killed M. tuberculosis-exposed isolated human NK cells. Brain levels of N-acetyl-L-alanine are decreased in a rat model of diabetic neuropathic pain induced by streptozotocin (STZ; Item No. 13104).² Increased urine levels of N-acetyl-L-alanine are associated with mutations in the gene encoding aminoacylase-1 (ACY1), an enzyme involved in the hydrolysis of N-acetylated proteins.³

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1. Yang, B., Mukherjee, T., Radhakrishnan, R., et al. HIV-differentiated metabolite N-acetyl-L-alanine dysregulates human natural killer cell responses to Mycobacterium tuberculosis infection. Int. J. Mol. Sci. 24(8), 7267 (2023).

2. Zhang, Q., Li, Q., Liu, S., et al. Decreased amino acids in the brain might contribute to the progression of diabetic neuropathic pain. Diabetes Res. Clin. Pract. 176, 108790. (2021).

3. Sass, J.O., Mohr, V., Olbrich, H., et al. Mutations in ACY1, the gene encoding aminoacylase 1, cause a novel inborn error of metabolism. Am. J. Hum. Genet. 78(3), 401-409 (2006).