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Higher-order oligomers, likely with a tetramer organization, are formed from dimers, the smallest unit suggested for TGR5 Y111A variants.
Data suggest that TGR5 and FXR (Montrer NR1H4 Protéines) in intestinal mucosa are important for glucose homeostasis, in particular in metabolic disorders such as type 2 diabetes and obesity. (TGR5 = membrane-type receptor for bile acids TGR5; FXR (Montrer NR1H4 Protéines) = farnesoid X receptor (Montrer xpr1 Protéines)) [REVIEW; Congress as Topic]
The authors conclude that taurodeoxycholic acid-induced DNA damage may depend on the activation of TGR5, CREB (Montrer CREB1 Protéines) and NOX5 (Montrer NOX5 Protéines)-S. It is possible that in Barrett's patients bile acids may activate NOX5 (Montrer NOX5 Protéines)-S and increase reactive oxygen species (ROS (Montrer ROS1 Protéines)) production via activation of TGR5 and CREB (Montrer CREB1 Protéines). NOX5 (Montrer NOX5 Protéines)-S-derived ROS (Montrer ROS1 Protéines) may cause DNA damage, thereby contributing to the progression from Barrett's esophagus to esophageal adenocarcinoma.
GPBAR1 is expressed in advanced gastric cancers and its expression correlates with markers of epithelial-mesenchymal transition
TGR5 activation induces mitochondrial biogenesis and prevents renal oxidative stress and lipid accumulation, establishing a role for TGR5 in inhibiting Kidney Disease in Obesity and Diabetes Mellitus.
TGR5 exhibits significantly higher expression in NSCLC tumor samples and facilitates the growth and metastasis of NSCLC by activating the JAK2 (Montrer JAK2 Protéines)/STAT3 (Montrer STAT3 Protéines) 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 (Montrer NFKB1 Protéines) 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.
TGR5 agonism induces NO production via Akt (Montrer AKT1 Protéines) activation and intracellular Ca(2 (Montrer CA2 Protéines)+) increase in vascular endothelial cells, and this function inhibits monocyte adhesion in response to inflammatory stimuli.
TGR5 has been linked to signaling pathways involved in metabolism, cell survival, proliferation and apoptosis, which suggest a possible role of TGR5 in cancer development.
G-protein coupled bile acid receptor 1 (TGR5) is required for cold-induced beiging of subcutaneous white adipose tissue (scWAT).
Work is the first to provide evidence for a TGR5-inhibited inflammatory response in ischemia/reperfusion injury through suppression of the TLR4 (Montrer TLR4 Protéines)-NF-kappaB (Montrer NFKB1 Protéines) 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 (Montrer NR1H4 Protéines) and TGR5 expression is down-regulated in aging kidney; caloric restriction prevents these age-related changes. Additionally, in long-lived Ames dwarf (Montrer PROP1 Protéines) mice, renal FXR (Montrer NR1H4 Protéines) and TGR5 expression is up-regulated. Treatment of aged mice with dual FXR (Montrer NR1H4 Protéines)/TGR5 agonist reverses age-related changes in kidney structure/function. (FXR (Montrer NR1H4 Protéines) = farnesoid X activated receptor (Montrer NR1H4 Protéines); 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 (Montrer NR1H4 Protéines) induces Tgr5 gene expression and increases Ca(2 (Montrer CA2 Protéines)+) levels and cAMP activity to stimulate GLP-1 (Montrer GCG Protéines) 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 (Montrer GCG Protéines) to GLP-1 (Montrer GCG Protéines) 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.
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