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Mouse Anti-NMNAT1 Recombinant Antibody (A1377) (CBMAB-AP5115LY)

The product is antibody recognizes NMNAT1. The antibody A1377 immunoassay techniques such as: Dot blot, ELISA, WB.
See all NMNAT1 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
A1377
Antibody Isotype
IgG2b, κ
Application
Dot blot, ELISA, WB

Basic Information

Immunogen
Recombinant human NMNAT1 (1-279aa) purified from E. coli
Specificity
Human
Antibody Isotype
IgG2b, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Purity
Affinity purity
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
Nicotinamide Nucleotide Adenylyltransferase 1
Introduction
This gene encodes an enzyme which catalyzes a key step in the biosynthesis of nicotinamide adenine dinucleotide (NAD). The encoded enzyme is one of several nicotinamide nucleotide adenylyltransferases, and is specifically localized to the cell nucleus. Activity of this protein leads to the activation of a nuclear deacetylase that functions in the protection of damaged neurons. Mutations in this gene have been associated with Leber congenital amaurosis 9. Alternative splicing results in multiple transcript variants. Pseudogenes of this gene are located on chromosomes 1, 3, 4, 14, and 15. [provided by RefSeq, Jul 2014]
Entrez Gene ID
64802
UniProt ID
Q9HAN9
Alternative Names
Nicotinamide Nucleotide Adenylyltransferase 1; Nicotinate-Nucleotide Adenylyltransferase 1; NMN/NaMN Adenylyltransferase 1; NaMN Adenylyltransferase 1; NMN Adenylyltransferase 1; NMNAT; Nicotinamide/Nicotinic Acid Mononucleotide Adenylyltransferase 1; Nicotinamide Mononucleotide Adenylyltransferase 1; Nicotinamide-Nucleotide 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).
Fails to cleave phosphorylated dinucleotides NADP+, NADPH and NaADP+ (PubMed:17402747).
Protects against axonal degeneration following mechanical or toxic insults (By similarity).
Biological Process
ATP generation from poly-ADP-D-riboseManual Assertion Based On ExperimentIDA:UniProtKB
NAD biosynthetic processManual Assertion Based On ExperimentIBA:GO_Central
Negative regulation of neuron deathIEA:Ensembl
Nucleotide biosynthetic process1 PublicationIC:UniProtKB
Response to woundingIEA:Ensembl
Cellular Location
Nucleus
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.
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.

Karim, M., Iqbal, T., Nawaz, A., Yaku, K., & Nakagawa, T. (2023). Deletion of Nmnat1 in Skeletal Muscle Leads to the Reduction of NAD+ Levels but Has No Impact on Skeletal Muscle Morphology and Fiber Types. Journal of Nutritional Science and Vitaminology, 69(3), 184-189.

Brown, E. E., Scandura, M. J., & Pierce, E. A. (2023). Expression of NMNAT1 in the photoreceptors is sufficient to prevent NMNAT1-associated retinal degeneration. Molecular Therapy-Methods & Clinical Development, 29, 319-328.

Iqbal, T., Nawaz, A., Karim, M., Yaku, K., Hikosaka, K., Matsumoto, M., & Nakagawa, T. (2022). Loss of hepatic Nmnat1 has no impact on diet-induced fatty liver disease. Biochemical and Biophysical Research Communications, 636, 89-95.

Shi, X., Jiang, Y., Kitano, A., Hu, T., Murdaugh, R. L., Li, Y., ... & Nakada, D. (2021). Nuclear NAD+ homeostasis governed by NMNAT1 prevents apoptosis of acute myeloid leukemia stem cells. Science advances, 7(30), eabf3895.

Sokolov, D., Sechrest, E. R., Wang, Y., Nevin, C., Du, J., & Kolandaivelu, S. (2021). Nuclear NAD+-biosynthetic enzyme NMNAT1 facilitates development and early survival of retinal neurons. Elife, 10, e71185.

Greenwald, S. H., Brown, E. E., Scandura, M. J., Hennessey, E., Farmer, R., Du, J., ... & Pierce, E. A. (2021). Mutant Nmnat1 leads to a retina-specific decrease of NAD+ accompanied by increased poly (ADP-ribose) in a mouse model of NMNAT1-associated retinal degeneration. Human Molecular Genetics, 30(8), 644-657.

Bedoni, N., Quinodoz, M., Pinelli, M., Cappuccio, G., Torella, A., Nigro, V., ... & Rivolta, C. (2020). An Alu-mediated duplication in NMNAT1, involved in NAD biosynthesis, causes a novel syndrome, SHILCA, affecting multiple tissues and organs. Human molecular genetics, 29(13), 2250-2260.

Sasaki, Y., Kakita, H., Kubota, S., Sene, A., Lee, T. J., Ban, N., ... & Milbrandt, J. (2020). SARM1 depletion rescues NMNAT1-dependent photoreceptor cell death and retinal degeneration. elife, 9, e62027.

Greenwald, S. H., Brown, E. E., Scandura, M. J., Hennessey, E., Farmer, R., Pawlyk, B. S., ... & Pierce, E. A. (2020). Gene therapy preserves retinal structure and function in a mouse model of NMNAT1-associated retinal degeneration. Molecular Therapy-Methods & Clinical Development, 18, 582-594.

Shi, X., Nakada, D., Kitano, A., Murdaugh, R., Tseng, Y. J., Hoegenauer, K., ... & Jiang, Y. (2019). Targeting NMNAT1 in Acute Myeloid Leukemia. Blood, 134, 879.

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For research use only. Not intended for any clinical use.

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