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novel role of let-7b/Fzd4 (show FZD4 ELISA Kits) axis through wnt (show WNT2 ELISA Kits) signaling
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 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.
Study shows that WNT5A (show WNT5A ELISA Kits) stimulates dimerization of membrane-anchored FZD4 (show FZD4 ELISA Kits) CRDs and oligomerization of full-length FZD4 (show FZD4 ELISA Kits), which requires the integrity of CRD (show CRX ELISA Kits) palmitoleoyl-binding residues. These results suggest that FZD receptors may form signalosomes in response to Wnt (show WNT2 ELISA Kits) binding through the CRDs and that the Wnt (show WNT2 ELISA Kits) palmitoleoyl group is important in promoting these interactions.
FZD4 (show FZD4 ELISA Kits) down-regulation leads to loss of WNT (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) signal activity and subsequently to reduced alveolar epithelial cell wound repair capacity and impaired expression of elastogenic components.
his study showed that Let7b modulates the proliferation, invasiveness, and migration of liver cancer cell and reduces the proportion of cancer stem cells in liver cancer cell by inhibiting Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) signaling pathway via downregulated Frizzled4 (show FZD4 ELISA Kits).
Among the detected mutations, LRP5 (show LRP5 ELISA Kits) accounted for the largest proportion with a mean mutation rate of 16.1% (5/31, 16.1%), followed by NDP (show NDP ELISA Kits) (3/31, 9.7%), FZD4 (show FZD4 ELISA Kits) (2/31, 6.5%), TSPAN12 (show TSPAN12 ELISA Kits) (1/31, 3.2%), and KIF11 (show KIF11 ELISA Kits) (1/31, 3.2%). All the novel changes were predicted to be pathogenic by a series of bioinformatics analyses.
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.
Work is the first to provide evidence for a TGR5-inhibited inflammatory response in ischemia/reperfusion injury through suppression of the TLR4 (show TLR4 ELISA Kits)-NF-kappaB (show 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 (show 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 (show PROP1 ELISA Kits) mice, renal FXR (show NR1H4 ELISA Kits) and TGR5 expression is up-regulated. Treatment of aged mice with dual FXR (show NR1H4 ELISA Kits)/TGR5 agonist reverses age-related changes in kidney structure/function. (FXR (show NR1H4 ELISA Kits) = farnesoid X activated receptor (show 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 (show NR1H4 ELISA Kits) induces Tgr5 gene expression and increases Ca(2 (show CA2 ELISA Kits)+) levels and cAMP activity to stimulate GLP-1 (show 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 (show GCG ELISA Kits) to GLP-1 (show 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 (show MLXIP ELISA Kits)-26a is a target gene of bile acid receptor (show NR1H4 ELISA Kits) GPBAR-1/TGR5
TGR5 agonism induces NO production via Akt (show AKT1 ELISA Kits) activation and intracellular Ca(2 (show CA2 ELISA Kits)+) 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.
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