Nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) is an enzyme that in humans is encoded by the NMNAT2gene.[5][6][7]
This gene product belongs to the nicotinamide-nucleotide adenylyltransferase (NMNAT) enzyme family, members of which catalyze an essential step in the nicotinamide adenine dinucleotide (NAD+ (NADP)) biosynthetic pathway. NMNAT2 is cytoplasmic (associated with the Golgi apparatus),[8] and is predominantly expressed in the brain. Two transcript variants encoding different isoforms have been found for this gene.[7]
Loss of NMNAT2 initiates Wallerian degeneration.[9] By contrast, NMNAT2 enhancement opposes the actions of SARM1 which would lead to axon degeneration,[10] but this effect is not due to preventing SARM1 depletion of NAD+.[9] Mice lacking NMNAT2 die before birth,[11] but are completely rescued by SARM1 deletion.[12] Activation of NMNAT2 by Sirtuin 3 (SIRT3) may be a means of inhibiting axon degeneration and dysfunction.[13]
^Raffaelli N, Sorci L, Amici A, Emanuelli M, Mazzola F, Magni G (Oct 2002). "Identification of a novel human nicotinamide mononucleotide adenylyltransferase". Biochem Biophys Res Commun. 297 (4): 835–40. doi:10.1016/S0006-291X(02)02285-4. PMID12359228.
Sorci L, Cimadamore F, Scotti S, et al. (2007). "Initial-rate kinetics of human NMN-adenylyltransferases: substrate and metal ion specificity, inhibition by products and multisubstrate analogues, and isozyme contributions to NAD+ biosynthesis". Biochemistry. 46 (16): 4912–22. doi:10.1021/bi6023379. PMID17402747.
