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Nicotinamide/nicotinic acid mononucleotide adenylyltransferase 1

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).

Involvement in disease

Leber congenital amaurosis 9

LCA9

A severe dystrophy of the retina, typically becoming evident in the first years of life. Visual function is usually poor and often accompanied by nystagmus, sluggish or near-absent pupillary responses, photophobia, high hyperopia and keratoconus.

None

The disease is caused by variants affecting the gene represented in this entry.

Spondyloepiphyseal dysplasia, sensorineural hearing loss, impaired intellectual development, and Leber congenital amaurosis

SHILCA

An autosomal recessive disorder characterized by early-onset retinal degeneration, sensorineural hearing loss, short stature due to spondyloepiphyseal dysplasia, and motor and intellectual delay. Brain imaging shows abnormalities including delayed myelination, leukoencephalopathy, and cerebellar hypoplasia.

None

The disease is caused by variants affecting the gene represented in this entry.

Pathway

Cofactor biosynthesis; NAD(+) biosynthesis; NAD(+) from nicotinamide D-ribonucleotide: step 1/1.

Cofactor biosynthesis; NAD(+) biosynthesis; deamido-NAD(+) from nicotinate D-ribonucleotide: step 1/1.

Sequence similarities

Belongs to the eukaryotic NMN adenylyltransferase family.

Tissue specificity

Widely expressed with highest levels in skeletal muscle, heart and kidney. Also expressed in the liver pancreas and placenta. Widely expressed throughout the brain.

Cellular localization

  • Nucleus

Alternative names

NMNAT, NMNAT1, Nicotinamide/nicotinic acid mononucleotide adenylyltransferase 1, NMN/NaMN adenylyltransferase 1, Nicotinamide-nucleotide adenylyltransferase 1, Nicotinate-nucleotide adenylyltransferase 1, NMN adenylyltransferase 1, NaMN adenylyltransferase 1

Target type

Proteins

Primary research area

Metabolism

Molecular weight

31932Da

We found 2 products in 2 categories

Assay Kits

Reactive species

Detection method

Proteins & Peptides

Species of origin

Search our catalogue for 'Nicotinamide/nicotinic acid mononucleotide adenylyltransferase 1' (2)

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