NIACR1 Antibody | 56-577

NIACR1 Antibody | 56-577 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human

Homology: Predicted species reactivity based on immunogen sequence: Mouse

Immunogen: This NIACR1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 200-228 amino acids from the Central region of human NIACR1.

Research Area: Cell Cycle, Obesity, Signal Transduction, Growth Factors

Tested Application: WB

Application: For WB starting dilution is: 1:1000

Specificiy: N/A

Positive Control 1: N/A

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: 42 kDa

Validation: N/A

Isoform: N/A

Purification: This antibody is purified through a protein A column, followed by peptide affinity purification.

Clonality: Polyclonal

Clone: N/A

Isotype: Rabbit Ig

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.

Concentration: batch dependent

Storage Condition: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

Alternate Name: Hydroxycarboxylic acid receptor 2, G-protein coupled receptor 109A, G-protein coupled receptor HM74A, Niacin receptor 1, Nicotinic acid receptor, HCAR2, GPR109A, HCA2, HM74A, NIACR1

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

BACKGROUND: NIACR1 acts as a high affinity receptor for both nicotinic acid (also known as niacin) and (D) -beta-hydroxybutyrate and mediates increased adiponectin secretion and decreased lipolysis through G (i) -protein-mediated inhibition of adenylyl cyclase. This pharmacological effect requires nicotinic acid doses that are much higher than those provided by a normal diet. Mediates nicotinic acid-induced apoptosis in mature neutrophils. Receptor activation by nicotinic acid results in reduced cAMP levels which may affect activity of cAMP-dependent protein kinase A and phosphorylation of target proteins, leading to neutrophil apoptosis. The rank order of potency for the displacement of nicotinic acid binding is 5-methyl pyrazole-3-carboxylic acid = pyridine-3-acetic acid > acifran > 5-methyl nicotinic acid = acipimox >> nicotinuric acid = nicotinamide.