Mouse Anti-NMNAT1 Recombinant Antibody (CBWJN-1453) (CBMAB-N2808-WJ)

Name: Mouse Anti-NMNAT1 Recombinant Antibody (CBWJN-1453)
SKU: CBMAB-N2808-WJ
Rating: 5 (1 reviews)

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Datasheet

SDS

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Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

CBWJN-1453

Application

IHC

Specificity

Human

Antibody Isotype

IgG2b

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

Lyophilized

Buffer

PBS, Trehalose

Storage

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

More Infomation

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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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
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For research use only. Not intended for any clinical use.

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