Nmnat2 (NM_001048042) Rat Tagged ORF Clone Lentiviral Particle
CAT#: RR214703L3V
- LentiORF®
Lenti ORF particles, Nmnat2 (Myc-DDK-tagged ORF) - Rat nicotinamide nucleotide adenylyltransferase 2 (Nmnat2), 200ul, >10^7 TU/mL
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CNY 7,410.00
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Specifications
Product Data | |
Product Name | Nmnat2 (NM_001048042) Rat Tagged ORF Clone Lentiviral Particle |
Vector | pLenti-C-Myc-DDK-P2A-Puro |
ACCN | NM_001048042 |
ORF Size | 921 bp |
Sequence Data |
The ORF insert of this clone is exactly the same as(RR214703).
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OTI Disclaimer | The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info |
OTI Annotation | This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene. |
Reference Data | |
RefSeq | NM_001048042.1, NP_001041507.1 |
RefSeq Size | 1239 bp |
RefSeq ORF | 924 bp |
Locus ID | 289095 |
Gene Summary | Nicotinamide/nicotinate-nucleotide adenylyltransferase that acts as an axon maintenance factor (By similarity). Catalyzes the formation of NAD(+) from nicotinamide mononucleotide (NMN) and ATP. Can also use the deamidated form; nicotinic acid mononucleotide (NaMN) as substrate but with a lower efficiency. Cannot use triazofurin monophosphate (TrMP) as substrate. Also catalyzes the reverse reaction, i.e. the pyrophosphorolytic cleavage of NAD(+). For the pyrophosphorolytic activity prefers NAD(+), NADH and NaAD as substrates and degrades nicotinic acid adenine dinucleotide phosphate (NHD) less effectively. Fails to cleave phosphorylated dinucleotides NADP(+), NADPH and NaADP(+) (By similarity). 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).[UniProtKB/Swiss-Prot Function] |
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