Part of Thermo Fisher Scientific

G Protein-Coupled Rec. 109B Polyclonal Antibody

G Protein-Coupled Rec. 109B Antibody for ELISA

Synonyms:
HM74, PUMAG, Puma-g
Entrez Gene ID:
(Human) 8843
UniProt ID:
P49019
Details
Host / Isotype: Rabbit
Class: Polyclonal
Type: Antibody
Species Reactivity: Human (Hu)
Immunogen: Synthetic peptide of human G protein-coupled receptor 109B.
Ordering Information
Pierce G Protein-Coupled Rec. 109B Polyclonal Antibody
Product Number Pkg. Size Price Purchase
GB-30097 100 µg $325.00
Add G Protein-Coupled Rec. 109B Polyclonal Antibody to your cart.

This product is not available outside of the U.S.

Storage: Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.
Form: 100 µg of affinity purified antibody. Supplied lyophilized. Reconstitute with 100 µl sterile water to restore original concentration 1 mg/ml (1X PBS).


Applications Dilution *
ELISA (ELISA) 1:5,000
* Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.
Product Specific Information
GB-30097 detects G Protein-Coupled Receptor HM74 in human samples.

GB-30097 has been successfully used in ELISA procedures.

The GB-30097 immunogen is a synthetic peptide located on the putative extracellular domain of human G protein-coupled receptor 109B.
General Information
Tunaru et al. (2003) showed that HM74 (GPR109B) s highly expressed in adipose tissue and is a nicotinic acid receptor. Binding of nicotinicacid to PUMA-G, the mouse ortholog, or to HM74, resulted in a G protein-mediated decrease in cAMP levels.
Nicotinic acid has been used for decades as alipid-lowering agent; Wise et al. (2003) and Tunaru et al. (2003) identified a G protein-coupled receptor that is highly expressed in adipose tissue and to which nicotinic acid is a high affinity ligand, thus identifying the cellular mechanism by which nicotinic acid exerts its main effect (i.e., suppression of lipolysis from adipose tissue). Karpe and Frayn (2004) discussed the implications of these findings and suggested that research on signaling through the nicotinic acid receptor might give rise to novel and more effective methods to interfere with fatty acid metabolism and a mechanism for the treatment of hyperlipidemia and possibly insulin-resistant states.
(This product is for In Vitro experimental use only. Not for resale without express authorization.)