NAPRT1 Antibody [H9L14] | Primary Antibodies

Application: Reactivity: Mouse, Human

Usage Information

Dilution
WB1:5000-1:50000 IHC1:20-1:200 IF1:100-1:500

Application
WB, IHC, IF

Reactivity
Mouse, Human

Source
Mouse Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
55 kDa 51 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
NAPRT1 Antibody [H9L14] detects endogenous levels of total NAPRT1 protein.

Clone
H9L14

Synonym(s)
Nicotinate phosphoribosyltransferase, NAPRTase, FHA-HIT-interacting protein, Nicotinate phosphoribosyltransferase domain-containing protein 1, NAPRT, FHIP, NAPRT1

Background
NAPRT1 (nicotinate phosphoribosyltransferase 1) is a cytosolic enzyme within the type II phosphoribosyltransferase family that initiates the nicotinic acid-dependent NAD salvage pathway by catalyzing the conversion of nicotinic acid and 5-phosphoribosyl-1-pyrophosphate into nicotinic acid mononucleotide, a precursor that is further processed to NAD. The protein forms a functional homodimer, with each subunit contributing conserved residues and metal-dependent contacts to the active site, creating a catalytic pocket specialized for the transfer of nicotinic acid onto the ribose-phosphate backbone. This enzymatic route maintains intracellular NAD levels independently of the parallel nicotinamide salvage pathway driven by NAMPT. Functional studies in human cells and tissues demonstrate that NAPRT1 activity increases NAD content, enhances mitochondrial membrane potential, and reduces reactive oxygen species accumulation during cellular stress, directly linking NAPRT1-mediated NAD biosynthesis to protection from oxidative injury. NAPRT1 is broadly distributed but variably expressed in normal tissues and tumors, with high expression in several epithelial tissues and some malignancies, while other tumors display low or absent expression due to promoter hypermethylation or alternative regulatory mechanisms, which determines the ability of cells to utilize nicotinic acid as an NAD precursor. In cancer models, cells lacking NAPRT1 are unable to synthesize NAD from nicotinic acid and become reliant on NAMPT for NAD production; inhibition of NAMPT in these cells leads to profound NAD depletion and cell death that cannot be rescued by nicotinic acid, whereas tumors with intact NAPRT1 expression can bypass NAMPT inhibition when supplemented with nicotinic acid.

Background

NAPRT1 (nicotinate phosphoribosyltransferase 1) is a cytosolic enzyme within the type II phosphoribosyltransferase family that initiates the nicotinic acid-dependent NAD salvage pathway by catalyzing the conversion of nicotinic acid and 5-phosphoribosyl-1-pyrophosphate into nicotinic acid mononucleotide, a precursor that is further processed to NAD. The protein forms a functional homodimer, with each subunit contributing conserved residues and metal-dependent contacts to the active site, creating a catalytic pocket specialized for the transfer of nicotinic acid onto the ribose-phosphate backbone. This enzymatic route maintains intracellular NAD levels independently of the parallel nicotinamide salvage pathway driven by NAMPT. Functional studies in human cells and tissues demonstrate that NAPRT1 activity increases NAD content, enhances mitochondrial membrane potential, and reduces reactive oxygen species accumulation during cellular stress, directly linking NAPRT1-mediated NAD biosynthesis to protection from oxidative injury. NAPRT1 is broadly distributed but variably expressed in normal tissues and tumors, with high expression in several epithelial tissues and some malignancies, while other tumors display low or absent expression due to promoter hypermethylation or alternative regulatory mechanisms, which determines the ability of cells to utilize nicotinic acid as an NAD precursor. In cancer models, cells lacking NAPRT1 are unable to synthesize NAD from nicotinic acid and become reliant on NAMPT for NAD production; inhibition of NAMPT in these cells leads to profound NAD depletion and cell death that cannot be rescued by nicotinic acid, whereas tumors with intact NAPRT1 expression can bypass NAMPT inhibition when supplemented with nicotinic acid.

References
https://pubmed.ncbi.nlm.nih.gov/25201160/ https://pubmed.ncbi.nlm.nih.gov/32266141/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

Tech Support

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%