抗Human GPBAR1 抗体:
抗Rat (Rattus) GPBAR1 抗体:
抗Mouse (Murine) GPBAR1 抗体:
Human Polyclonal GPBAR1 Primary Antibody for IHC (p) - ABIN4359103
Alemi, Poole, Chiu, Schoonjans, Cattaruzza, Grider, Bunnett, Corvera: The receptor TGR5 mediates the prokinetic actions of intestinal bile acids and is required for normal defecation in mice. in Gastroenterology 2012
Human Polyclonal GPBAR1 Primary Antibody for ICC, IF - ABIN4247420
Mikó, Vida, Kovács, Ujlaki, Trencsényi, Márton, Sári, Kovács, Boratkó, Hujber, Csonka, Antal-Szalmás, Watanabe, Gombos, Csoka, Kiss, Vígh, Szabó, Méhes, Sebestyén, Goedert, Bai: Lithocholic acid, a bacterial metabolite reduces breast cancer cell proliferation and aggressiveness. in Biochimica et biophysica acta. Bioenergetics 2018
Human Monoclonal GPBAR1 Primary Antibody for CyTOF, FACS - ABIN4899058
Yoneno, Hisamatsu, Shimamura, Kamada, Ichikawa, Kitazume, Mori, Uo, Namikawa, Matsuoka, Sato, Koganei, Sugita, Kanai, Hibi: TGR5 signalling inhibits the production of pro-inflammatory cytokines by in vitro differentiated inflammatory and intestinal macrophages in Crohn's disease. in Immunology 2013
The newly synthesized analogues were evaluated on human orthologs of FXR and GPBAR1 receptors in a luciferase reporter assay..FXR selectivity is a critical point in the pharmacological claim of FXR agonists in cholestasis disorders, where the concomitant activation of GPBAR1 limits the pharmacological utility of dual agonists.
Activation of FXR inhibits, whereas TGR5 activation may promote, cholangiocarcinoma progression by regulating proliferation, migration and mitochondrial energy metabolism.
RYGB increased circulating bile acids, ileal Takeda G protein-coupled receptor 5 (TGR5) and mTORC1 signaling activity, as well as GLP-1 production in both mice and human subjects. Inhibition of ileal mTORC1 signaling by rapamycin significantly attenuated the stimulation of bile acid secretion, TGR5 expression and GLP-1 synthesis induced by RYGB in lean and diet-induced obese mice.
TGR5 is strongly expressed in collecting ducts, distal convoluted tubules and thin loop of Henle. TGR5 protein and mRNA expression were notably decreased in clear cell renal cell carcinomas and may be helpful in differentiating these tumors from other renal cell carcinomas.
The findings suggest that activation of TGR5 promoted mitochondrial biogenesis in endothelial cells, which is mediated by the CREB/PGC-1a signaling pathway.
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 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 = farnesoid X receptor) [REVIEW; Congress as Topic]
The authors conclude that taurodeoxycholic acid-induced DNA damage may depend on the activation of TGR5, CREB and NOX5-S. It is possible that in Barrett's patients bile acids may activate NOX5-S and increase reactive oxygen species (ROS) production via activation of TGR5 and CREB. NOX5-S-derived ROS 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/STAT3 signaling pathway.
TGR5 may have a role in the progression from Barrett's Esophagus to high-grade dysplasia and esophageal adenocarcinoma
contributes to hepatic cystogenesis by increasing cAMP and enhancing cholangiocyte proliferation
anti-inflammation therapy targeting Gpbar1/NF-kappaB 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 expression is significantly associated with bile acid receptors VDR and TGR5 expression. Our studies identify a novel role of a tight junction protein 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) modulatory activity.
TGR5 agonism induces NO production via Akt activation and intracellular Ca(2+) 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.
bile acid signaling through TGR5 is not required for the beneficial effects of (RYGB) Roux en-Y Gastric Bypass in the mouse and that RYGB and vertical sleeve gastrectomy may achieve their similar beneficial effects through different mechanisms.
The unconjugated bile acids CDCA, DCA and UDCA and, to a lesser extent, CA were found to be relatively potent agonists for the GPBAR1 (TGR5) receptor and elicit cAMP release, whereas all glyco- and tauro- conjugated bile acids are weak agonists.
our data reveal a positive feedback loop regulating IRF3 signaling and suggest a potential therapeutic role for metabolite-sensing GPCRs in controlling viral diseases.
In summary, both TGR5 and FXR regulate multiple complementary as well as nonoverlapping signaling andmetabolic pathways that are important for the pathogenesis and prevention of diabetic nephropathy.
The obtained results provide a new insight into the physiological function of TGR5 in bone formation.
Tgr5 contributes to improved muscle function
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-NF-kappaB 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 and TGR5 expression is down-regulated in aging kidney; caloric restriction prevents these age-related changes. Additionally, in long-lived Ames dwarf mice, renal FXR and TGR5 expression is up-regulated. Treatment of aged mice with dual FXR/TGR5 agonist reverses age-related changes in kidney structure/function. (FXR = farnesoid X activated receptor; 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 induces Tgr5 gene expression and increases Ca(2+) levels and cAMP activity to stimulate GLP-1 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 to GLP-1 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-26a is a target gene of bile acid receptor GPBAR-1/TGR5
Impaired Itching Perception in Murine Models of Cholestasis Is Supported by Dysregulation of GPBAR1 Signaling
Data show that the action of bile acids on -like peptide-1 (GLP-1) secretion is predominantly mediated by G protein-coupled bile acid receptor GPBAR1 (TGR5) located on the basolateral L-cell membrane.
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