Anti-Human NMNAT1 Antibody Pair

Product Description: Nicotinamide nucleotide adenylyltransferase 1 (NMNAT1) is a nuclear enzyme that catalyzes a crucial step in the biosynthesis of nicotinamide adenine dinucleotide (NAD+), converting nicotinamide mononucleotide (NMN) and ATP into NAD+ and pyrophosphate, a reaction essential for cellular metabolism and energy homeostasis. NMNAT1 exhibits transferase and nucleotidyltransferase activity, binding nucleotides and ATP, and is strongly inhibited by certain polyphenols such as gallotannin. The protein is highly conserved and plays a protective role in neuronal cells, notably delaying axonal degeneration after injury, although its axon-protective function is less robust than that of the related Wld(S) protein. Clinically, mutations in NMNAT1 are linked to Leber's congenital amaurosis type 9 (LCA9), a severe inherited retinal dystrophy that leads to early-onset vision loss. Additionally, NMNAT1 expression declines with age in several tissues, potentially impacting NAD+ metabolism and age-related cellular functions. Protein Function: Catalyzes the formation of NAD(+) from nicotinamide mononucleotide (NMN) and ATP (PubMed:17402747). Can also use the deamidated form, nicotinic acid mononucleotide (NaMN) as substrate with the same efficiency (PubMed:17402747). Can use triazofurin monophosphate (TrMP) as substrate (PubMed:17402747). Also catalyzes the reverse reaction, i.e. the pyrophosphorolytic cleavage of NAD(+) (PubMed:17402747). For the pyrophosphorolytic activity, prefers NAD(+) and NaAD as substrates and degrades NADH, nicotinic acid adenine dinucleotide phosphate (NHD) and nicotinamide guanine dinucleotide (NGD) less effectively (PubMed:17402747). Involved in the synthesis of ATP in the nucleus, together with PARP1, PARG and NUDT5 (PubMed:27257257). Nuclear ATP generation is required for extensive chromatin remodeling events that are energy-consuming (PubMed:27257257). Also acts as a cofactor for glutamate and aspartate ADP-ribosylation by directing PARP1 catalytic activity to glutamate and aspartate residues on histones (By similarity). Fails to cleave phosphorylated dinucleotides NADP(+), NADPH and NaADP(+) (PubMed:17402747). Protects against axonal degeneration following mechanical or toxic insults (By similarity). Neural protection does not correlate with cellular NAD(+) levels but may still require enzyme activity (By similarity) [The Uniprot Consortium]