NMNAT2 (human) (rec.) (His)
|Synonyms||Nicotinamide Mononucleotide Adenylyltransferase 2; NMN Adenylyltransferase 2; NaMN Adenylyltransferase 2|
|Sequence||Human NMNA2 (aa 2-307) is fused at the N-terminus to a His-tag.|
|Concentration||0.1mg/ml after reconstitution.|
|Reconstitution||Reconstitute with 100μl sterile water.|
|Formulation||Lyophilized in 55mM TRIS-Cl, pH 8.2, containing 150mM NaCl plus 0.025% CHAPS.|
|Other Product Data||UniProt link Q9BZQ4: NMNAT2 (human)|
|Shipping and Handling|
|Short Term Storage||+4°C|
|Long Term Storage||-20°C|
After reconstitution, prepare aliquots and store at -20°C.
Avoid freeze/thaw cycles.
Centrifuge lyophilized vial before opening and reconstitution.
Stable for at least 6 months after receipt when stored at -20°C.
Working aliquots are stable for up to 3 months when stored at -20°C.
|Product Specification Sheet|
Nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) catalyzes the formation of NAD+ from nicotinamide mononucleotide (NMN) and ATP. Can also use the deamidated form nicotinic acid mononucleotide (NaMN) as a substrate but with lower efficiency. NMNAT2 also catalyzes the reverse reaction, i.e. the pyrophosphorolytic cleavage of NAD+. It is highly expressed in brain, in particular in cerebrum, cerebellum, occipital lobe, frontal lobe, temporal lobe and putamen. NMNAT2 is also found in the heart, skeletal muscle, pancreas and islets of Langerhans. NMNAT2 is essential for axon growth and survival. Its loss from injured axons may activate Wallerian degeneration (axon degeneration induced by nerve injury), whereas NMNAT overexpression rescues axons from degeneration.