Human Recombinant NMNAT1 protein, His Tag (V2LY-0526-LY5811)

Name: Human Recombinant NMNAT1 protein, His Tag
SKU: V2LY-0526-LY5811
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

Expressed Host

Baculovirus-Insect Cells

Protein Species

Human

Tag

His Tag

Protein Construction

This product is Human Recombinant NMNAT1 protein, His Tag consist of Amino Acid: 1-279 and predicts a molecular mass of 33.38 kDa.

Molecule Mass

33.38 kDa

Sequence

Amino Acid: 1-279

Species

Human

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

Purity

>85% as determined by SDS-PAGE

Endotoxin

Please contact us for more information.

Format

Lyophilized

Reconstitution

Allow the vial and reconstitution buffer to equilibrate to room temperature. Briefly centrifuge or tap down the vial to ensure that all lyophilized powder is collected at the bottom of the vial. For the reconstitution of this product, we recommend adding PBS or sterile water to achieve a final antibody concentration of 1 mg/mL. Allow the vial to reconstitute for 10-15 minutes at room temperature with gentle agitation. Avoid vigorous shaking that can cause foaming and antibody denaturation. Aliquot into volumes based on your experiment and store liquid protein at -20°C or -80°C for long time.

Buffer

Lyophilized from sterile PBS

Preservative

None

Storage

Samples are stable for up to twelve months from date of receipt at -20°C to -80°C. Store it under sterile conditions at -20°C to -80°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.

More Infomation

Target

Full Name

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

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