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TGR5 may have a role in the progression from Barrett's Esophagus to high-grade dysplasia and esophageal adenocarcinoma
anti-inflammation therapy targeting Gpbar1/NF-kappaB (show NFKB1 Proteins) pathway could be effective in suppressing bile acid-induced inflammation and alleviating Intrahepatic cholestasis of pregnancy-associated fetal disorders.
human TGR5 (hTGR5) shows higher nomilin responsiveness than does mouse TGR5.
bile acids promote intestinal epithelial cell proliferation and decrease mucosal injury by upregulating TGR5 expression in obstructive jaundice.
The generated contour maps revealed the important structural insights for the activity of the compounds. The results obtained from this study could be helpful in the development of novel and more potent agonists of TGR5.
TGR5 functions as a tumor-suppressor in patients with ampullary adenocarcinoma and preoperative hyperbilirubinemia
We conclude that Claudin-2 (show CLDN2 Proteins) expression is significantly associated with bile acid receptors VDR (show CYP27B1 Proteins) and TGR5 expression. Our studies identify a novel role of a tight junction protein (show OCLN Proteins) in the development and progression of esophageal mucosal metaplasia, dysplasia and carcinoma.
this is the first report of bile acid derivatives able to antagonize GPBAR1 and and farnesoid X receptor (show xpr1 Proteins) (FXR (show NR1H4 Proteins)) modulatory activity.
These findings identify TGR5 as a suppressor of gastric cancer cell proliferation and migration
Because elevated levels of circulatory LPS (show IRF6 Proteins) may contribute to the development of insulin (show INS Proteins) resistance, the results from this study suggest that bile acids through the activation of TGR5 may have a role in the development of insulin (show INS Proteins) resistance as well.
TGR5 agonism induces NO production via Akt (show AKT1 Proteins) activation and intracellular Ca(2 (show CA2 Proteins)+) increase in vascular endothelial cells, and this function inhibits monocyte adhesion in response to inflammatory stimuli.
Work is the first to provide evidence for a TGR5-inhibited inflammatory response in ischemia/reperfusion injury through suppression of the TLR4 (show TLR4 Proteins)-NF-kappaB (show NFKB1 Proteins) pathway.
findings show GPBAR1 is essential for maintaining intestinal immune homeostasis and that its activation in the setting of inflammation reverses the immune dysfunction that occurs in rodent models of colitis
Data suggest that FXR (show NR1H4 Proteins) and TGR5 expression is down-regulated in aging kidney; caloric restriction prevents these age-related changes. Additionally, in long-lived Ames dwarf (show PROP1 Proteins) mice, renal FXR (show NR1H4 Proteins) and TGR5 expression is up-regulated. Treatment of aged mice with dual FXR (show NR1H4 Proteins)/TGR5 agonist reverses age-related changes in kidney structure/function. (FXR (show NR1H4 Proteins) = farnesoid X activated receptor (show NR1H4 Proteins); TGR5 = G protein-coupled bile acid receptor 1)
GPBAR1/TGR5 receptor agonist, tauroursodeoxycholic acid, has anti-inflammatory effects in microglial cells.
Vertical sleeve gastrectomy achieves its postoperative therapeutic effects through enhanced TGR5 signaling.
These results suggest that TGR5 contributes to the glucoregulatory benefits of vertical sleeve gastrectomy surgery by promoting metabolically favourable shifts in the circulating bile acid pool.
findings uncovered a novel mechanism in which INT-767 activation of FXR (show NR1H4 Proteins) induces Tgr5 gene expression and increases Ca(2 (show CA2 Proteins)+) levels and cAMP activity to stimulate GLP-1 (show GCG Proteins) secretion and improve hepatic glucose and lipid metabolism in high-fat diet-induced obese mice.
The results suggest that TGR5 activation mediates cross-talk between alpha- and beta-cells by switching from glucagon (show GCG Proteins) to GLP-1 (show GCG Proteins) to restore beta- cell mass and function under hyperglycemic conditions.
TGR5 is an important mediator of bile acid-induced cholangiocyte proliferation in vivo and in vitro. Furthermore, TGR5 protects cholangiocytes from death receptor-mediated apoptosis.
miR (show MLXIP Proteins)-26a is a target gene of bile acid receptor (show NR1H4 Proteins) GPBAR-1/TGR5
This gene encodes a member of the G protein-coupled receptor (GPCR) superfamily. This enzyme functions as a cell surface receptor for bile acids. Treatment of cells expressing this GPCR with bile acids induces the production of intracellular cAMP, activation of a MAP kinase signaling pathway, and internalization of the receptor. The receptor is implicated in the suppression of macrophage functions and regulation of energy homeostasis by bile acids. Alternative splicing results in multiple transcript variants encoding the same protein.
G-protein coupled bile acid receptor 1
, G-protein coupled bile acid receptor BG37
, G-protein coupled receptor GPCR19
, membrane bile acid receptor
, membrane-type receptor for bile acids
, G protein-coupled receptor TGR5
, G protein-coupled receptor
, G protein-coupled bile acid receptor 1