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anti-Human BRS3 Antibodies:
anti-Mouse (Murine) BRS3 Antibodies:
anti-Rat (Rattus) BRS3 Antibodies:
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mammalian homologue of CCHa2-R, Bombesin receptor subtype-3 (Brs3), is an orphan receptor (show NR1D2 Antibodies) that is expressed in the islet beta-cells
High BRS3 expression is associated with liver metastases of pancreas neuroendocrine tumors.
The role of the human BRS-3 receptor in glucose homeostasis.
Data show that gastrin-releasing peptide receptor/bombesin receptor (show GRPR Antibodies) subtype-3 positive cells and protein expression in tumors decreased by treatment with RC-3095 or gemcitabine alone or greater in combination.
BRS-3 plays an important role in glucose metabolism.
BRS-3 agonist-dependent signaling mediates CREB (show CREB1 Antibodies) phosphorylation and transactivation through protein kinase (show CDK7 Antibodies) (PK)A, (PK)C, and mitogen-activated protein/extracellular regulated kinase kinase (MEK)-1 (show MAP2K1 Antibodies) pathways.
These results identify a potential role for BRS-3 in islet physiology, with agonism directly promoting glucose-stimulated insulin (show INS Antibodies) secretion
results indicate that the sequence variation in the E3 loop is responsible for the species difference between rat and human BRS-3, and multiple residues in the E3 loop are involved in interactions with the agonist dY-bombesin
Study found that the BRS-3 agonist stimulated adhesion of NCI-N417 cells in laminin-coated culture wells suggesting that BRS-3 may be involved in invasion and metastasis of certain cancer cells
Data suggest that activator protein 2alpha and peroxisome-proliferator-activated receptor alpha (show PPARA Antibodies) may be especially involved in the ozone-inducible up-regulation mechanism of bombesin receptor subtype 3 expression.
Data suggest that the failure to detect an existing endogenous bombesin-like receptor 3 (BRS-3) ligand in the parabiotic mice could be due to limited cross-circulation and a ligand's short half-life.
Data from knockout mice suggest that Brs3 involvement in regulation of body temperature is via a central mechanism, upstream of sympathetic efferent pathways to stimulate brown adipose tissue.
This sstudy demonistrated comprehensive mapping of BRS-3 mRNA in the mouse brain and double in situ hybridization was performed to determine whether BRS-3 colocalizes with other neurotransmitters or neuropeptides.
Data suggest that the bombesin receptor subtype-3 agonist indirectly inhibited orexin (show OX Antibodies) neurons through GABAergic input and directly activated orexin (show OX Antibodies) neurons.
BRS-3-deficient mice remained longer in the open arms of the maze. Analyses of risk assessment behavior revealed that BRS-3-deficient mice exhibited increased 'stretched attend posture' behavior in both the L-D box and elevated plus maze tests.
BRS-3 genes were expressed from embryonic days 13-16 and on multiple postnatal days for lungs
BRS-3 gene deletion upsets the mechanism by which leptin (show LEP Antibodies) decreases the expression of MCH (show PMCH Antibodies)-R.
Hyperphagia is a major factor leading to increased body weight and hyperinsulinemia in BRS-3 KO mice.
The protein encoded by this gene is a G protein-coupled membrane receptor that binds bombesin-like peptides. This binding results in activation of a phosphatidylinositol-calcium second messenger system, with physiological effects including regulation of metabolic rate, glucose metabolism, and hypertension.
bombesin receptor subtype-3
, bombesin-like peptide receptor subtype 3.5
, bombesin-like receptor subtype 3
, bombesin-like receptor 3
, bombesin receptor subtype-3-like
, G-protein coupled receptor
, bombesin receptor subtype 3