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Loss of FXR or its down-regulation is associated with higher bile acids concentrations and with a pro-tumorigenic phenotype. (Review)
Lys (show LYZ Proteins)-325 is a non-canonical site of SUMOylation of human FXR.CK2 is the priming effector that phosphorylates Ser (show SIGLEC1 Proteins)-327, resulting in enhanced SUMO2 (show SUMO2 Proteins) conjugation, which then directs the ubiquitination and degradation of FXR through the recruitment of the SUMO-dependent ubiquitin E3 ligase RNF4 (show RNF4 Proteins).
we proposed a model to link FXR to Sp1 (show PSG1 Proteins), which included triggered FXR, p38/MAPK (show MAPK14 Proteins) and/or PI3K (show PIK3CA Proteins)/AKT (show AKT1 Proteins) signaling and phosphorylated Sp1 (show PSG1 Proteins), to illustrate the potential crosstalk between the two factors.
the presented evidence suggested that WA can inhibit HCC (show FAM126A Proteins) cell proliferationand tumorigenesis through miR (show MLXIP Proteins)-22-repressed CCNA2 (show CCNA2 Proteins), which was at least partially through FXR regulation
The results indicated that epigenetically regulated miR (show MLXIP Proteins)-449a targets CREB5 (show CREB5 Proteins) to increase FXRalpha expression, thereby promoting HBV replication and gene expression. Our findings provide a new understanding of the role of miRNAs in HBV replication
In diabetic humans, there is decreased FXR expression in the kidney. FXR plays an important role in Diabetic Kidney Disease.
FXR regulates serum triglyceride level in part through PLA2G12B (show PLA2G12B Proteins).
we conclude that FXR-Gank (show PSMD10 Proteins)-TSPs-Stem cells pathway is a key determinant of liver cancer in animal models and in pediatric liver cancer. Our data provide a strong basis for development of FXR-Gank (show PSMD10 Proteins)-based therapy for treatment of patients with hepatoblastoma
PPARalpha (show PPARA Proteins) and FXR function coordinately to integrate liver energy balance.
These studies investigated in differentiated HepaRG cells and in primary human hepatocytes (PHHs) effects of FXR activation on HBV replication and of infection on the FXR pathway.
results suggest that hypothyroidism induces a moderate non-alcoholic steatohepatitis, alllowing the hepatic regeneration. The FXRalpha may be involved in the development of non-alcoholic steatohepatitis in hypothyroid subjects.
FXR is expressed in the ovary, in all regions of the oviduct, and all portions of the vagina of rabbits.
FXR signaling is a bile acid nuclear receptor that regulates lipids and glucose homeostasis and lack of it causes hepatomegaly and liver dysfunction.
These results suggest that lack of FXR impaired FoxO3a (show FOXO3 Proteins)-mediated autophagy and in turn exacerbated alcohol-induced liver injury
Bile acids and salts (BA) treatment-farnesoid X-activated receptor (FRXalpha) signaling is a critical actor during sexual maturation.
The study shows that FXR/RXR regulates Chop (show DDIT3 Proteins) expression in a mouse model of steatohepatitis, providing novel insights into pathogenesis of this disorder.
FXR activation ameliorated central nervous system autoimmunity in an IL-10 (show IL10 Proteins)-dependent fashion and even suppressed advanced clinical disease upon therapeutic administration
In livers of mice, FXR regulates amino acid catabolism and detoxification of ammonium via ureagenesis and glutamine synthesis.
Data suggest that FXR and TGR5 (show GPBAR1 Proteins) 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 and TGR5 (show GPBAR1 Proteins) expression is up-regulated. Treatment of aged mice with dual FXR/TGR5 (show GPBAR1 Proteins) agonist reverses age-related changes in kidney structure/function. (FXR = farnesoid X activated receptor; TGR5 (show GPBAR1 Proteins) = G protein-coupled bile acid receptor 1 (show GPBAR1 Proteins))
this study provides evidence for roles of FXR as an important regulator of placental inflammation
These findings suggest that bile acids and FXR play pivotal roles in sepsis via controlling the NLRP3 (show NLRP3 Proteins) inflammasome.
alterations in bile acid composition may have contributed to the observed disturbance in FXR-mediated signalling pathways in short bowel syndrome-associated liver disease
FXR splice variant has a dominant positive effect on wild type FXR.
In conclusion, PXR (show NR1I2 Proteins) and FXR both responded to ligands that activated their human orthologs, and some of the alternatively spliced variants significantly altered PXR (show NR1I2 Proteins) and FXR transactivation at in vivo expression levels.
This gene encodes a ligand-activated transcription factor, which shares structural features in common with nuclear hormone receptor family, such as a DNA-binding domain that targets the receptor to specific DNA sequences, and a ligand-binding domain, which interacts directly with the ligand and contains a ligand-dependent transcriptional activation domain. This protein functions as a receptor for bile acids, and when bound to bile acids, regulates the expression of genes involved in bile acid synthesis and transport. Alternatively spliced transcript variants encoding different isoforms have been described for this gene.
nuclear receptor subfamily 1, group H, member 4
, orphan nuclear receptor FOR2
, bile acid receptor
, farnesoid X activated receptor
, bile acid receptor-like
, RXR-interacting protein 14
, farnesoid X nuclear receptor
, farnesoid X-activated receptor
, farnesol receptor HRR-1
, retinoid X receptor-interacting protein 14
, nuclear receptor subfamily 1 group H member 4