Nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) is an enzyme that in humans is encoded by the NMNAT2 gene.[5][6][7]
AliasesNMNAT2, C1orf15, PNAT2, nicotinamide nucleotide adenylyltransferase 2 Quick facts Identifiers, Aliases ...
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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]
The catechin epigallocatechin gallate (EGCG) found in tea can activate NMNAT2 by more than 100%.[14]
