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Key Documents

WH0023057M1

Sigma-Aldrich

Monoclonal Anti-NMNAT2 antibody produced in mouse

clone 2E4, purified immunoglobulin, buffered aqueous solution

Synonyme(s) :

Nmnat2 Antibody, Nmnat2 Antibody - Monoclonal Anti-NMNAT2 antibody produced in mouse, Anti-C1orf15, Anti-KIAA0479, Anti-MGC2756, Anti-PNAT2, Anti-nicotinamide nucleotide adenylyltransferase 2

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

mouse

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

2E4, monoclonal

Forme

buffered aqueous solution

Espèces réactives

human

Technique(s)

indirect ELISA: suitable
western blot: 1-5 μg/mL

Isotype

IgG1κ

Numéro d'accès GenBank

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... NMNAT2(23057)

Description générale

NMNAT2 (nicotinamide nucleotide adenylyltransferase 2) is a rate limiting enzyme that is located on human chromosome 1q25. It is expressed in the brain. Nmnat2 is located to vesicular structures.
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)

Immunogène

NMNAT2 (NP_055854, 208 a.a. ~ 307 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.

Sequence
CIPGLWNEADMEVIVGDFGIVVVPRDAADTDRIMNHSSILRKYKNNIMVVKDDINHPMSVVSSTKSRLALQHGDGHVVDYLSQPVIDYILKSQLYINASG

Application

Monoclonal Anti-NMNAT2 antibody has been used in immunoblotting.

Actions biochimiques/physiologiques

NMNAT2 (nicotinamide nucleotide adenylyltransferase 2) plays a major role in cancer suppression. It may induce multiplication and prevent apoptosis in CRC (colorectal cancer) cells. NMNAT2 participates in energy metabolism. This protein helps to postpone axon degeneration.

Forme physique

Solution in phosphate buffered saline, pH 7.4

Informations légales

GenBank is a registered trademark of United States Department of Health and Human Services

Clause de non-responsabilité

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Code de la classe de stockage

10 - Combustible liquids

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Équipement de protection individuelle

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

Rescue of peripheral and CNS axon defects in mice lacking NMNAT2
Gilley J, et al.
The Journal of Neuroscience, 33(33), 13410-13424 (2013)
Nmnat2 attenuates Tau phosphorylation through activation of PP2A
Cheng XS, et al.
Journal of Alzheimer'S Disease, 36(1), 185-195 (2013)
Nicotinamide Mononucleotide Adenylyl Transferase 2: A Promising Diagnostic and Therapeutic Target for Colorectal Cancer
Cui C, et al.
BioMed Research International, 2016 (2016)
Decreased SMG7 expression associates with lupus-risk variants and elevated antinuclear antibody production
Annals of the Rheumatic Diseases, 75(11) (2016)
Andrea Loreto et al.
Neurobiology of disease, 134, 104678-104678 (2019-11-20)
Wallerian degeneration of physically injured axons involves a well-defined molecular pathway linking loss of axonal survival factor NMNAT2 to activation of pro-degenerative protein SARM1. Manipulating the pathway through these proteins led to the identification of non-axotomy insults causing axon degeneration

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