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Mouse Anti-NMNAT2 Recombinant Antibody (B-10) (CBMAB-N2818-WJ)

This product is a Mouse antibody that recognizes NMNAT2. The antibody B-10 can be used for immunoassay techniques such as: WB, IP, IF, ELISA.
See all NMNAT2 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
B-10
Application
WB, IP, IF, ELISA

Basic Information

Specificity
Human
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!]

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

Target

Full Name
nicotinamide nucleotide adenylyltransferase 2
Introduction
This gene product belongs to the nicotinamide mononucleotide adenylyltransferase (NMNAT) enzyme family, members of which catalyze an essential step in NAD (NADP) biosynthetic pathway. Unlike the other human family member, which is localized to the nucleus, and is ubiquitously expressed; this enzyme is cytoplasmic, and is predominantly expressed in the brain. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]
Entrez Gene ID
23057
UniProt ID
Q9BZQ4
Alternative Names
Nicotinamide Nucleotide Adenylyltransferase 2; Nicotinamide Mononucleotide Adenylyltransferase 2; Nicotinate-Nucleotide Adenylyltransferase 2; NMN/NaMN Adenylyltransferase 2; NaMN Adenylyltransferase 2; NMN Adenylyltransferase 2; C1orf15; Nicotinamide/Nicotinic Acid Mononucleotide Adenylyltransferase 2;
Function
Nicotinamide/nicotinate-nucleotide adenylyltransferase that acts as an axon maintenance factor (By similarity).
Catalyzes the formation of NAD+ from nicotinamide mononucleotide (NMN) and ATP (PubMed:16118205, PubMed:17402747).
Can also use the deamidated form; nicotinic acid mononucleotide (NaMN) as substrate but with a lower efficiency (PubMed:16118205, PubMed:17402747).
Cannot use triazofurin monophosphate (TrMP) as substrate (PubMed:16118205, PubMed:17402747).
Also catalyzes the reverse reaction, i.e. the pyrophosphorolytic cleavage of NAD+ (PubMed:16118205, PubMed:17402747).
For the pyrophosphorolytic activity prefers NAD+, NADH and NaAD as substrates and degrades nicotinic acid adenine dinucleotide phosphate (NHD) less effectively (PubMed:16118205, PubMed:17402747).
Fails to cleave phosphorylated dinucleotides NADP+, NADPH and NaADP+ (PubMed:16118205, PubMed:17402747).
Axon survival factor required for the maintenance of healthy axons: acts by delaying Wallerian axon degeneration, an evolutionarily conserved process that drives the loss of damaged axons (By similarity).
Biological Process
NAD biosynthetic processManual Assertion Based On ExperimentIBA:GO_Central
Nucleotide biosynthetic process1 PublicationIC:UniProtKB
Cellular Location
Golgi apparatus membrane
Cytoplasmic vesicle membrane
Cytoplasm
Cell projection, axon
Delivered to axons with Golgi-derived cytoplasmic vesicles.
PTM
Degraded in response to injured neurite. Degradation is probably caused by ubiquitination by MYCBP2 (By similarity).
Ubiquitinated on threonine and/or serine residues by MYCBP2; consequences of threonine and/or serine ubiquitination are however unclear (PubMed:29643511).
Palmitoylated; palmitoylation is required for membrane association.

Yang, S., Niou, Z. X., Enriquez, A., LaMar, J., Huang, J. Y., Ling, K., ... & Lu, H. C. (2024). NMNAT2 supports vesicular glycolysis via NAD homeostasis to fuel fast axonal transport. Molecular Neurodegeneration, 19(1), 13.

Li, W., Gao, M., Hu, C., Chen, X., & Zhou, Y. (2023). NMNAT2: An important metabolic enzyme affecting the disease progression. Biomedicine & Pharmacotherapy, 158, 114143.

Chen, H., Zhang, X., Liao, N., Ji, Y., Mi, L., Gan, Y., ... & Wen, F. (2023). Downregulation of SIRT6 and NMNAT2 is associated with proliferative diabetic retinopathy. Molecular Vision, 29, 160.

Fang, F., Zhuang, P., Feng, X., Liu, P., Liu, D., Huang, H., ... & Hu, Y. (2022). NMNAT2 is downregulated in glaucomatous RGCs, and RGC-specific gene therapy rescues neurodegeneration and visual function. Molecular Therapy, 30(4), 1421-1431.

Cheng, X. S., Shi, F. X., Zhao, K. P., Lin, W., Li, X. Y., Zhang, J., ... & Zhou, X. W. (2021). Nmnat2 attenuates amyloidogenesis and up-regulates ADAM10 in AMPK activity-dependent manner. Aging (Albany NY), 13(20), 23620.

Loreto, A., Hill, C. S., Hewitt, V. L., Orsomando, G., Angeletti, C., Gilley, J., ... & Coleman, M. P. (2020). Mitochondrial impairment activates the Wallerian pathway through depletion of NMNAT2 leading to SARM1-dependent axon degeneration. Neurobiology of disease, 134, 104678.

Lukacs, M., Gilley, J., Zhu, Y., Orsomando, G., Angeletti, C., Liu, J., ... & Stottmann, R. W. (2019). Severe biallelic loss-of-function mutations in nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) in two fetuses with fetal akinesia deformation sequence. Experimental neurology, 320, 112961.

Huppke, P., Wegener, E., Gilley, J., Angeletti, C., Kurth, I., Drenth, J. P., ... & Coleman, M. P. (2019). Homozygous NMNAT2 mutation in sisters with polyneuropathy and erythromelalgia. Experimental Neurology, 320, 112958.

Gilley, J., Mayer, P. R., Yu, G., & Coleman, M. P. (2019). Low levels of NMNAT2 compromise axon development and survival. Human molecular genetics, 28(3), 448-458.

Wu, X., Hu, F., Zeng, J., Han, L., Qiu, D., Wang, H., ... & Wang, Q. (2019). NMNAT2‐mediated NAD+ generation is essential for quality control of aged oocytes. Aging cell, 18(3), e12955.

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

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