NAGS Antibody | 30-708

NAGS Antibody | 30-708 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse, Rat, Dog

Homology: N/A

Immunogen: Antibody produced in rabbits immunized with a synthetic peptide corresponding a region of human NAGS.

Research Area: Signal Transduction

Tested Application: E, WB

Application: NAGS antibody can be used for detection of NAGS by ELISA at 1:312500. NAGS antibody can be used for detection of NAGS by western blot at 1.25 μg/mL, and HRP conjugated secondary antibody should be diluted 1:50, 000 - 100, 000.

Specificiy: N/A

Positive Control 1: Cat. No. 1211 - HepG2 Cell Lysate

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: 58 kDa

Validation: N/A

Isoform: N/A

Purification: Antibody is purified by protein A chromatography method.

Clonality: Polyclonal

Clone: N/A

Isotype: N/A

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.

Concentration: batch dependent

Storage Condition: For short periods of storage (days) store at 4˚C. For longer periods of storage, store NAGS antibody at -20˚C. As with any antibody avoid repeat freeze-thaw cycles.

Alternate Name: NAGS, AGAS, ARGA, MGC133025

User Note: Optimal dilutions for each application to be determined by the researcher.

BACKGROUND: NAGS is a mitochondrial enzyme that catalyzes the formation of N-acetylglutamate (NAG) from glutamate and acetyl coenzyme-A. NAG is a cofactor of carbamyl phosphate synthetase I (CPSI) , the first enzyme of the urea cycle in mammals. Deficiencies in N-acetylglutamate synthase have been associated with hyperammonemia.The N-acetylglutamate synthase gene encodes a mitochondrial enzyme that catalyzes the formation of N-acetylglutamate (NAG) from glutamate and acetyl coenzyme-A. NAG is a cofactor of carbamyl phosphate synthetase I (CPSI) , the first enzyme of the urea cycle in mammals. This gene may regulate ureagenesis by altering NAG availability and, thereby, CPSI activity. Deficiencies in N-acetylglutamate synthase have been associated with hyperammonemia.