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N-acetyltransferase 8 like

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Target not currently curated in GtoImmuPdb

Target id: 3144

Nomenclature: N-acetyltransferase 8 like

Family: 2.3.1.- Acyltransferases

Gene and Protein Information Click here for help
Species TM AA Chromosomal Location Gene Symbol Gene Name Reference
Human 1 302 4p16.3 NAT8L N-acetyltransferase 8 like
Mouse 1 299 5 B2 Nat8l N-acetyltransferase 8-like
Rat 1 299 14q21 Nat8l N-acetyltransferase 8-like
Previous and Unofficial Names Click here for help
CML3 | aspartate N-acetyltransferase | ANAT
Database Links Click here for help
Ensembl Gene
Entrez Gene
Human Protein Atlas
KEGG Enzyme
RefSeq Nucleotide
RefSeq Protein
Enzyme Reaction Click here for help
EC Number: Acetyl-CoA + L-aspartate <=> CoA + N-acetyl-L-aspartate (NAA)

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Key to terms and symbols View all chemical structures Click column headers to sort
Ligand Sp. Action Value Parameter Reference
compound 5 [Stecula et al., 2020] Small molecule or natural product Hs Inhibition 6.4 pKi 3
pKi 6.4 (Ki 4x10-7 M) [3]
Physiological Consequences of Altering Gene Expression Click here for help
Knockout of the nat8l gene eliminates the brain defects that are the hallmark of human Canavan disease (ASPA deficiency).
Species:  Mouse
Tissue:  Brain
Technique:  Constitutive gene-knockout
References:  1-2
Gene Expression and Pathophysiology Comments
This enzyme is being examined as a potential druggable target for patients with Canavan disease, which is a rare neurodegenerative demyelinating disease that is caused by inherited loss-of-function mutation of aspartoacylase (ASPA; aminoacylase 2). ASPA defiiciency leads to accumulation of the critical brain metabolite N-acetyl-L-aspartate (NAA) and this is primarily responsible for the neurodegenerative symptoms of Canavan disease. Inhibitors of the N-acetyltransferase activity of NAT8L are predicterd to offer clinical utility by reversing the effect of ASPA deficiency by converting the abnormal load of NAA to L-aparagine in Canavan disease patients [3].


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1. Guo F, Bannerman P, Mills Ko E, Miers L, Xu J, Burns T, Li S, Freeman E, McDonough JA, Pleasure D. (2015) Ablating N-acetylaspartate prevents leukodystrophy in a Canavan disease model. Ann Neurol, 77 (5): 884-8. [PMID:25712859]

2. Sohn J, Bannerman P, Guo F, Burns T, Miers L, Croteau C, Singhal NK, McDonough JA, Pleasure D. (2017) Suppressing N-Acetyl-l-Aspartate Synthesis Prevents Loss of Neurons in a Murine Model of Canavan Leukodystrophy. J Neurosci, 37 (2): 413-421. [PMID:28077719]

3. Stecula A, Hussain MS, Viola RE. (2020) Discovery of Novel Inhibitors of a Critical Brain Enzyme Using a Homology Model and a Deep Convolutional Neural Network. Journal of Medicinal Chemistry, [Epub ahead of print]. DOI: 10.1021/acs.jmedchem.0c00473

How to cite this page

2.3.1.- Acyltransferases: N-acetyltransferase 8 like. Last modified on 03/08/2020. Accessed on 22/05/2024. IUPHAR/BPS Guide to PHARMACOLOGY,