GPR3 Antibody | 5175

GPR3 Antibody | 5175 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse, Rat

Homology: N/A

Immunogen: GPR3 antibody was raised against a 13 amino acid synthetic peptide from near the carboxy terminus of human GPR3.
The immunogen is located within the last 50 amino acids of GPR3.

Research Area: Neuroscience

Tested Application: E, WB, IHC-P, IF

Application: GPR3 antibody can be used for detection of GPR3 by Western blot at 1 - 2 μg/mL. Antibody can also be used for immunohistochemistry starting at 2.5 μg/mL. For immunofluorescence start at 20 μg/mL.
Antibody validated: Western Blot in mouse samples; Immunohistochemistry in human samples and Immunofluorescence in human samples. All other applications and species not yet tested.

Specificiy: N/A

Positive Control 1: Cat. No. 1287 - EL4 Cell Lysate

Positive Control 2: Cat. No. 10-901 - Human Spleen Tissue Slide

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: Predicted: 36 kDa
Observed: 36 kDa

Validation: N/A

Isoform: N/A

Purification: GPR3 Antibody is affinity chromatography purified via peptide column.

Clonality: Polyclonal

Clone: N/A

Isotype: IgG

Conjugate: Unconjugated

Physical State: Liquid

Buffer: GPR3 Antibody is supplied in PBS containing 0.02% sodium azide.

Concentration: 1 mg/mL

Storage Condition: GPR3 antibody can be stored 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: GPR3 Antibody: ACCA, ACCA, G-protein coupled receptor 3, ACCA orphan receptor

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

BACKGROUND: GPR3 Antibody: GPR3, also known as ACCA, is a G-protein coupled receptor that constitutively activates adenylate cyclase and is highly expressed in the central nervous system. Overexpression of GPR3 stimulates the production of amyloid-beta peptide (Abeta) , the deposition of which is one of the pathological hallmarks of Alzheimer 's disease (AD) , while the ablation of GPR3 prevented the accumulation of Abeta in vitro and in an AD mouse model. This is of particular interest because of the proximity of a reported candidate Alzheimer 's disease (AD) locus, suggesting that GPR3 may be a potential therapeutic target for the treatment of AD. GPR3 has also been shown to block the proliferation of cerebellar granule cell precursors (GCP) during postnatal development by inhibiting the Shh-induced proliferation of GCP, indicating that GPR3 activation may represent one of the signals that triggers the postnatal cell cycle exit and terminal differentiation of GPCs.