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Recombinant Human NMNAT2/NMNAT-2 Protein (His Tag) | PKSH031131

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SKU:
575-PKSH031131
Weight:
1.00 KGS
€1,133.00
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Description

Recombinant Human NMNAT2/NMNAT-2 Protein (His Tag) | PKSH031131 | Gentaur US, UK & Europe Disrtribition

Synonyms: C1orf15;PNAT2

Active Protein: N/A

Activity: A DNA sequence encoding the human NMNAT2 (Q9BZQ4-1)(Met1-Gly307) was fused with a polyhistide tag at the C-terminus.

Protein Construction: A DNA sequence encoding the human NMNAT2 (Q9BZQ4-1)(Met1-Gly307) was fused with a polyhistide tag at the C-terminus.

Fusion Tag: C-His

Species: Human

Expressed Host: Baculovirus-Insect Cells

Shipping: This product is provided as lyophilized powder which is shipped with ice packs.

Purity: > 90 % as determined by reducing SDS-PAGE.

Endotoxin: < 1.0 EU per µg as determined by the LAL method.

Stability and Storage: Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months.

Molecular Mass: 35.8 kDa

Formulation: Lyophilized from sterile 20mM Tris, 500mM NaCl, 5mM DTT, 10% glycerol, pH 8.0

Reconstitution: Please refer to the printed manual for detailed information.

Background: NMNAT2, also known as NMNAT-2, belongs to the nicotinamide mononucleotide adenylyltransferase (NMNAT) enzyme family. NMNAT is a central enzyme in NAD+ biosynthesis, transferring the adenylyl moiety of ATP to nicotinamide mononucleotide (NMN) or nicotinic acid mononucleotide (NaMN) resulting in the formation of NAD+ or NaAD+ and the release of pyrophosphate. NMNAT2 is predominantly expressed in human pancreas, insulinoma as well as in the brain, especially in the cerebrum, cerebellum, occipital lobe, frontal lobe, temporal lobe and putamen. Immunofluorescence microscopy localized endogenous NMNAT2 to the Golgi apparatus in human cell line. Endogenous NMNAT2 seem to be a labile axon survival factor, because specific depletion of NMNAT2 is sufficient to induce Wallerian-like degeneration of uninjured axons which endogenous NMNAT1 and NMNAT3 cannot prevent. Thus endogenous NMNAT2 represents an exciting new therapeutic target for axonal disorders.

Research Area: N/A

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