NMNAT2 (Vector pUC, Accession No. BC020998)

Length: 909 Sequence: atggaaatcc aggaactaga ggaaattcag gcctgccagg ggctctggga agtgtttgtt actctctcag aaagagccag ggattatctg cacaaaactg gaaggtttat tgtgattggc gggattgtct cccctgtcca cgactcctat ggaaaacagg gcctcgtgtc aagccggcac cgtctcatca tgtgtcagct ggccgtccag aattctgatt ggatcagggt ggacccttgg gagtgctacc aggacacctg gcagacgacc tgcagcgtgt tggaacacca ccgggacctc atgaagaggg tgactggctg catcctctcc aatgtcaaca caccttccat gacacctgtg atcggacagc cacaaaacga gaccccccag cccatttacc agaacagcaa cgtggccacc aagcccactg cagccaagat cttggggaag gtgggagaaa gcctcagccg gatctgctgt gtccgcccgc cggtggagcg tttcaccttt gtagatgaga atgccaatct gggcacggtg atgcggtatg aagagattga gctacggatc ctgctgctgt gtggtagtga cctgctggag tccttctgca tcccagggct ctggaacgag gcagatatgg aggtgattgt tggtgacttt gggattgtgg tggtgccccg ggatgcagcc gacacagacc gaatcatgaa tcactcctca atactccgca aatacaaaaa caacatcatg gtggtgaagg atgacatcaa ccatcccatg tctgttgtca gctcaaccaa gagcaggctg gccctgcagc atggggacgg ccatgttgtg gattacctgt cccagccggt catcgactac atcctcaaaa gccagctgta catcaatgcc Protein function: Nicotinamide/nicotinate-nucleotide adenylyltransferase that acts as an axon maintenance factor. Catalyzes the formation of NAD(+) from nicotinamide mononucleotide (NMN) and ATP (PubMed:16118205, PubMed:17402747). Can also use the deamidated form, nicotinic acid mononucleotide (NaMN) as substrate but with a lower efficiency (PubMed:16118205, PubMed:17402747). Cannot use triazofurin monophosphate (TrMP) as substrate (PubMed:16118205, PubMed:17402747). Also catalyzes the reverse reaction, i.e. the pyrophosphorolytic cleavage of NAD(+) (PubMed:16118205, PubMed:17402747). For the pyrophosphorolytic activity prefers NAD(+), NADH and NaAD as substrates and degrades nicotinic acid adenine dinucleotide phosphate (NHD) less effectively (PubMed:16118205, PubMed:17402747). Fails to cleave phosphorylated dinucleotides NADP(+), NADPH and NaADP(+) (PubMed:16118205, PubMed:17402747). Axon survival factor required for the maintenance of healthy axons: acts by delaying Wallerian axon degeneration, an evolutionarily conserved process that drives the loss of damaged axons. [The UniProt Consortium]