Human G Protein Coupled Receptor 109B (GPR109B) Protein

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Description
Human G Protein Coupled Receptor 109B (GPR109B) Protein is a recombinant Human protein expressed in E. coli.
Documents del producto
Product specifications
| Category | Proteins and Peptides |
| Immunogen Target | G Protein Coupled Receptor 109B (GPR109B) |
| Host | E. coli |
| Assay Type | Activity: Not tested Sequence Fragment: Please enquire. Tag: N-terminal His tag |
| Origin | Human |
| Conjugation | Unconjugated |
| Expression | Recombinant |
| Purity | > 90% |
| Size 1 | 10 µg |
| Size 2 | 50 µg |
| Size 3 | 100 µg |
| Size 4 | 200 µg |
| Size 5 | 500 µg |
| Form | Lyophilized |
| Tested Applications | WB, SDS-PAGE |
| Buffer | Prior to lyophilization: PBS, pH 7.4, containing 0.01% Sarcosyl, 1 mM DTT, 5% Trehalose and Proclin-300. |
| Availability | Shipped within 5-7 working days. |
| Storage | Store lyophilized form at 2-8°C for up to 1 month. For longer periods, store lyophilized or liquid at -80°C. Avoid repeated freeze–thaw cycles. |
| Dry Ice | No |
| Alias | HCAR3,NIACR2,Low affinity nicotinic acid receptor,Nic2,G protein-coupled receptor 109B,GPR109B,HCA3,HM74, PUMAG,Puma-g |
| Background | Protein HCAR3 |
| Status | RUO |
| Note | THIS PRODUCT IS FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC, THERAPEUTIC OR COSMETIC PROCEDURES. NOT FOR HUMAN OR ANIMAL CONSUMPTION. To keep the original salt concentration, we recommend reconstituting to the original concentration prior to lyophilization (see Concentration) in ddH2O. If a lower concentration is required, dilute in PBS, pH 7.4. If a higher concentration is required, the product can be reconstituted directly in PBS, pH 7.4, though please note that this will change the overall salt concentration. The stock concentration should be between 0.1-1.0 mg/ml. Do not vortex. Concentration: Prior to lyophilization: 200 µg/ml |
Descripción
HCAR3, also known as GPR109B, is a G protein-coupled receptor closely related to HCAR2 and activated by nicotinic acid and specific long-chain fatty acid derivatives. It is primarily expressed in adipose tissue, immune cells, and skin, where it regulates lipid metabolism, inflammation, and immune responses. Similar to HCAR2, HCAR3 activation inhibits cAMP production through Gi/o proteins, leading to the suppression of lipolysis and decreased free fatty acid release. HCAR3 has been linked to lipid and energy homeostasis, particularly in regulating triglyceride levels and promoting energy storage. In immune cells, HCAR3 signaling mediates anti-inflammatory effects, contributing to the resolution of inflammation and tissue repair. While its physiological roles are less characterized compared to HCAR2, HCAR3 is emerging as a potential target for metabolic and inflammatory diseases. HCAR3 expression in the skin has also been associated with niacin-induced flushing, a side effect relevant to lipid-lowering therapies. Its involvement in lipid regulation and immune modulation makes HCAR3 a candidate for therapeutic interventions targeting metabolic and inflammatory disorders.
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