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Validated All-in-One™ qPCR Primer for NR1H4(NM_001206979.2) Search again
Product ID:
HQP167317
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BAR, FXR, HRR-1, HRR1, PFIC5, RIP14
Gene Description:
nuclear receptor subfamily 1 group H member 4
Target Gene Accession:
NM_001206979.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Gene References into function
- Amino acids asparagine 354 and isoleucine 372 of Farnesoid X activated receptor are critical to its function
- These results provide molecular evidence for a cross-talk between the FXR and PPARalpha pathways in humans.
- role in regulating syndecan-1 expression
- FXR regulates bile acid amidation, a critical component of the enterohepatic circulation of bile acids
- kininogen is a novel and direct target of farnesoid X receptor
- Farnesoid X receptor (FXR) induces the UGT2B4 enzyme in hepatocytes; this study identifies UGT2B4 as a novel FXR target gene.
- demonstrated that FGF-19, acting as an FXR-induced signaling molecule, represses expression of the CYP7A1 gene; this signaling cascade defines a novel mechanism for feedback repression of bile acid biosynthesis
- bile acid and synthetic activators of the nuclear FXR as negative regulators of Apo CIII expression.
- MDR3 expression is directly up-regulated by FXR in primary human hepatocytes
- the existence of an auto-regulatory loop in FXR signaling pathways: the binding of each bile acid results in a different FXR conformations, which in turn differentially regulates expression of individual FXR targets
- Loss of familial intrahepatic cholestasis-1 leads to diminished nuclear translocation of FXR, with subsequent potential for pathologic alterations in intestinal and hepatic bile acid transporter expression.
- FXR is expressed in a variety of normal and pathological human tissue
- FXR is activated by DRIP205, which modulates the bile acid response of its target genes
- PGC-1alpha mediates the ligand-dependent activation of FXR and transcription of SHP gene.
- Hepatic down-regulation of Farnesoid X receptor contributes to severety of familial intrahepatic cholestasis.
- FXR has a central role in lipid homeostasis
- presence of two functional FXR recognition sites located in a 345-bp element within the 5'-flanking region of CYP3A4
- studies provide evidence that farnesoid X-receptor(FXR) directly recruits specific chromatin modifying activity of co-activator-associated arginine methyltransferase 1 (CARM1) necessary for full potentiation of bile salt export pump (BSEP) locus in vivo
- farnesoid X receptor regulates carbohydrate metabolism
- the coordinate regulation of FXR target genes is lost in cerebrotendinous xanthomatosis
- complement C3 expression is regulated by the bile acid receptor FXR
- The FXR isoforms were recently identified that differ either at their N termini and/or by the presence of four amino acids in the hinge region.
- activation of FXR may suppress glycolysis and enhance oxidation of fatty acids via inactivation of the pyruvate dehydrogenase complex by increasing PDK4 expression
- FXR-mediated activation of ICAM-1 could be further enhanced by TNF-alpha cotreatment in hepatocytes
- Induction of alpha A crystallin expression in response to bile acid-activated FXR contributes to cellular defense against bile acid-induced hepatotoxicity
- FXR agonists may increase gallbladder fluid secretion through transcriptional activation of VPAC1.
- These results show that the stimulation of ASCT2 expression in response to glutamine in part involves binding of FXR/RXR to the ASCT2 promoter.
- overexpression of human OSTalpha and OSTbeta facilitated the uptake of conjugated chenodeoxycholate and the activation of FXR target genes
- OSTalpha/OSTbeta expression is induced by bile acids through ligand-dependent transactivation of both OST genes by the nuclear bile acid receptor/farnesoid X receptor (FXR).
- These results indicate that expression of Ostalpha and Ostbeta are highly regulated in response to cholestasis and that this response is dependent on the FXR bile acid receptor.
- FXR is a potential therapeutic target for the treatment and prevention of numerous metabolic and lipid-related diseases
- The results obtained using truncated PGC-1alpha proteins suggested that two regions are necessary for PGC-1alpha to interact with the DNA-binding complex of RXRalpha/FXR.
- Taken together, these results suggest that activation of FXR plays a critical role in regulating adipogenesis and insulin signaling.
- The farnesoid X receptor (FXR) was detected in normal and tumor breast tissue, with a high level of expression in ductal epithelial cells of normal breast and infiltrating ductal carcinoma cells.
- The bile acid receptor FXR is significantly overexpressed in Barrett's esophagus compared to normal mucosa, esophagitis and esophageal adenocarcinoma.
- an SP2/KLF6 repression complex by SHP is required for farnesoid X receptor-induced endothelial cell migration
- The use of human liver slices in nuclear receptor metabolism research is reported; the farnesoid X receptor system was chosen as a model.
- FXR is expressed in breast cancer interacts with ER
- farnesoid X receptor exerts metabolic control beyond bile acid homeostasis, notably effects on HDL, triglyceride and glucose metabolism [review]
- analysis of the 5'-flanking region of human FXR gene in HepG2 cells
- Expression levels of FXR target genes are significantly reduced in livers harboring an FXR*1B allele.
- Functional variants of FXR may predispose to intrahepatic cholestasis of pregnancy.
- summarize the current knowledge of the functions regulated by bile acids and how their physiological receptors,FXR, mediate the signaling underlying numerous cellular responses
- in three ethnically distinct populations there is a complex interaction of fxr alleles and other risk factors for the development of cholelithiasis
- Expression of FXR in normal and cancer prostate epithelial cells and its activation by chenodeoxycholic acid.
- FXR is expressed and induces its target gene SHP in VSMCs, and activation of FXR and SHP lead to downregulation of important contributors to vascular inflammation and migration, notably COX-2 and iNOS.
- FXR has a role in modulating liver cell apoptosis
- FXR appears to induce decorin expression at a transcriptional level.
- FIC1 signals to FXR via PKC zeta. FIC1-related liver disease is likely related to downstream effects of FXR on bile acid homeostasis.
- The data strongly suggest that FXRalpha is another member of the nuclear receptor superfamily implicated in the regulation of HBV core promoter activity and that bile acids could play an important role in the natural history of HBV infection.
- FXR is a new transcription factor of GLUT4, further elucidating the potential role for FXR in glucose metabolism.
- massively secreted biliary cholesterol from macrophages suppressed the expression of CYP7 proteins in a farnesoid X receptor (FXR)-dependent manner in HepG2 cells.
- p300 acts as a critical coactivator of FXR induction of SHP by acetylating histones at the promoter and FXR itself
- the role of genetic variants in FXR itself, FXR target genes, and regulators of FXR in the pathophysiology of the liver and intestine has become increasingly evident--REVIEW
- Potential role of FXR-mediated NF-kappaB inhibition for pathogenesis and treatment of liver diseases.
- Report antiatherosclerotic effect of farnesoid X receptor.
- In human adrenal cells, FXR increases transcription and expression of HSD3B2.
- FXR agonists and/or modulators may prove to be clinically useful for treating non-alcoholic fatty liver.