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TGR5 exhibits significantly higher expression in NSCLC tumor samples and facilitates the growth and metastasis of NSCLC by activating the JAK2 (zeige JAK2 ELISA Kits)/STAT3 (zeige STAT3 ELISA Kits) signaling pathway.
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 (zeige NFKB1 ELISA Kits) 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 (zeige CLDN2 ELISA Kits) expression is significantly associated with bile acid receptors VDR (zeige CYP27B1 ELISA Kits) and TGR5 expression. Our studies identify a novel role of a tight junction protein (zeige OCLN ELISA Kits) 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 (FXR (zeige NR1H4 ELISA Kits)) modulatory activity.
These findings identify TGR5 as a suppressor of gastric cancer cell proliferation and migration
TGR5 agonism induces NO production via Akt (zeige AKT1 ELISA Kits) activation and intracellular Ca(2 (zeige CA2 ELISA Kits)+) 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 (zeige TLR4 ELISA Kits)-NF-kappaB (zeige NFKB1 ELISA Kits) 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 (zeige NR1H4 ELISA Kits) and TGR5 expression is down-regulated in aging kidney; caloric restriction prevents these age-related changes. Additionally, in long-lived Ames dwarf (zeige PROP1 ELISA Kits) mice, renal FXR (zeige NR1H4 ELISA Kits) and TGR5 expression is up-regulated. Treatment of aged mice with dual FXR (zeige NR1H4 ELISA Kits)/TGR5 agonist reverses age-related changes in kidney structure/function. (FXR (zeige NR1H4 ELISA Kits) = farnesoid X activated receptor (zeige NR1H4 ELISA Kits); 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 (zeige NR1H4 ELISA Kits) induces Tgr5 gene expression and increases Ca(2 (zeige CA2 ELISA Kits)+) levels and cAMP activity to stimulate GLP-1 (zeige GCG ELISA Kits) 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 (zeige GCG ELISA Kits) to GLP-1 (zeige GCG ELISA Kits) 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 (zeige MLXIP ELISA Kits)-26a is a target gene of bile acid receptor (zeige NR1H4 ELISA Kits) 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