Rat Bile Acid Receptor (NR1H4) ELISA Kit | BAR elisa kit

Rat Bile Acid Receptor (NR1H4) ELISA Kit

Cat. Num. AAA9712682

• Gene Names: Nr1h4; Fxr
• Reactivity: Rat
• Synonyms: Bile Acid Receptor (NR1H4); Rat Bile Acid Receptor (NR1H4) ELISA Kit; NR1H4; FXR; HRR-1; HRR1; MGC163445; RIP14; farnesoid X receptor; BAR elisa kit

• Reactivity: Rat
• Specificity: Rat Bile acid receptor (NR1H4) ELISA Kit has high sensitivity and excellent specificity for detection of Rat NR1H4. No significant cross-reactivity or interference between Rat NR1H4 and analogues was observed.
• Sequence Length: 469

• Assay Type: Sandwich ELISA (Quantitative)
• Samples: Cell Culture Supernatants, Serum, Plasma, Other Biological Fluids
• Detection Method: Colorimetric
• Usage Notes: * Do not mix components from different kit lots or use reagents beyond the kit expiration date.; * Allow all reagents to warm to room temperature for at least 30 minutes before opening.; * Pre-rinse the pipet tip with reagent, use fresh pipet tips for each sample, standard and reagent to avoid contamination.; * Unused wells must be kept desiccated at 4 degree C in the sealed bag provided.; * Mix Thoroughly is very important for the result. It is recommended using low frequency oscillator or slight hand shaking every 10 minutes.; * It is recommended that all samples and standards be assayed in duplicate or triplicate.
• Preparation and Storage: Store at 2-8 degree C.

Typical Testing Data/Standard Curve (for reference only)

(Fig.1. Rat Bile acid receptor (NR1H4) Standard Curve.)

Related Product Information for BAR elisa kit

Description: This Rat Bile acid receptor (NR1H4) ELISA Kit employs a two-site sandwich ELISA to quantitate NR1H4 in samples. An antibody specific for NR1H4 has been pre-coated onto a microplate. Standards and samples are pipetted into the wells and any NR1H4 present is bound by the immobilized antibody. After removing any unbound substances, a biotin-conjugated antibody specific for NR1H4 is added to the wells. After washing, Streptavidin conjugated Horseradish Peroxidase (HRP) is added to the wells. Following a wash to remove any unbound avidin-enzyme reagent, a substrate solution is added to the wells and color develops in proportion to the amount of NR1H4 bound in the initial step. The color development is stopped and the intensity of the color is measured.

Background: The farnesoid X receptor (FXR),is a nuclear hormone receptor with activity similar to that seen in other steroid receptors such as estrogen or progesterone but more similar in form to PPAR, LXR and RXR. FXR is encoded by the NR1H4 gene.FXR is expressed at high levels in the liver and intestine. Chenodeoxycholic acid and other bile acids are natural ligands for FXR. Like other steroid receptors, when activated, FXR translocates to the cell nucleus, forms a dimer (in this case a heterodimer with RXR) and binds to hormone response elements on DNA which elicits expression or transrepression of gene products.

NCBI and Uniprot Product Information

• NCBI GI #: 11120690
• NCBI GeneID: 60351
• NCBI Accession #: NP_068513.1
• NCBI GenBank Nucleotide #: NP_068513.1
• UniProt Accession #: Q62735
• NCBI Official Full Name: bile acid receptor
• NCBI Official Synonym Full Names: nuclear receptor subfamily 1, group H, member 4
• NCBI Official Symbol: Nr1h4
• NCBI Official Synonym Symbols: Fxr
• NCBI Protein Information: bile acid receptor
• UniProt Protein Name: Bile acid receptor
• Protein Family: Barbiturase
• UniProt Gene Name: Nr1h4
• UniProt Synonym Gene Names: Bar; Fxr; Rip14; RXR-interacting protein 14

NCBI Description

nuclear hormone receptor that is activated by farnesol metabolites [RGD, Feb 2006]

Uniprot Description

Ligand-activated transcription factor. Receptor for bile acids (BAs) such as chenodeoxycholic acid (CDCA), lithocholic acid, deoxycholic acid (DCA) and allocholic acid (ACA). Plays a essential role in BA homeostasis through the regulation of genes involved in BA synthesis, conjugation and enterohepatic circulation. Also regulates lipid and glucose homeostasis and is involved innate immune response. The FXR-RXR heterodimer binds predominantly to farnesoid X receptor response elements (FXREs) containing two inverted repeats of the consensus sequence 5'-AGGTCA-3' in which the monomers are spaced by 1 nucleotide (IR-1) but also to tandem repeat DR1 sites with lower affinity, and can be activated by either FXR or RXR-specific ligands. It is proposed that monomeric nuclear receptors such as NR5A2/LRH-1 bound to coregulatory nuclear responsive element (NRE) halfsites located in close proximity to FXREs modulate transcriptional activity. In the liver activates transcription of the corepressor NR0B2 thereby indirectly inhibiting CYP7A1 and CYP8B1 (involved in BA synthesis) implicating at least in part histone demethylase KDM1A resulting in epigenomic repression, and SLC10A1/NTCP (involved in hepatic uptake of conjugated BAs). Activates transcription of the repressor MAFG (involved in regulation of BA synthesis). Activates transcription of SLC27A5/BACS and BAAT (involved in BA conjugation), ABCB11/BSEP (involved in bile salt export) by directly recruiting histone methyltransferase CARM1, and ABCC2/MRP2 (involved in secretion of conjugated BAs) and ABCB4 (involved in secretion of phosphatidylcholine in the small intestine). Activates transcription of SLC27A5/BACS and BAAT (involved in BA conjugation), ABCB11/BSEP (involved in bile salt export) by directly recruiting histone methyltransferase CARM1, and ABCC2/MRP2 (involved in secretion of conjugated BAs) and ABCB4 (involved in secretion of phosphatidylcholine in the small intestine). In the intestine activates FGF19 expression and secretion leading to hepatic CYP7A1 repression. The function also involves the coordinated induction of hepatic KLB/beta-klotho expression. Regulates transcription of liver UGT2B4 and SULT2A1 involved in BA detoxification; binding to the UGT2B4 promoter seems to imply a monomeric transactivation independent of RXRA. Modulates lipid homoestasis by activating liver NR0B2/SHP-mediated repression of SREBF1 (involved in de novo lipogenesis), expression of PLTP (involved in HDL formation), SCARB1 (involved in HDL hepatic uptake), APOE, APOC1, APOC4, PPARA (involved in beta-oxidation of fatty acids), VLDLR and SDC1 (involved in the hepatic uptake of LDL and IDL remnants), and inhibiting expression of MTTP (involved in VLDL assembly). Increases expression of APOC2 (promoting lipoprotein lipase activity implicated in triglyceride clearance). Transrepresses APOA1 involving a monomeric competition with NR2A1 for binding to a DR1 element. Also reduces triglyceride clearance by inhibiting expression of ANGPTL3 and APOC3 (both involved in inhibition of lipoprotein lipase). Involved in glucose homeostasis by modulating hepatic gluconeogenesis through activation of NR0B2/SHP-mediated repression of respective genes. Modulates glycogen synthesis (inducing phosphorylation of glycogen synthase kinase-3). Modulates glucose-stimulated insulin secretion and is involved in insulin resistance. Involved in intestinal innate immunity. Plays a role in protecting the distal small intestine against bacterial overgrowth and preservation of the epithelial barrier. Down-regulates inflammatory cytokine expression in several types of immune cells including macrophages and mononuclear cells. Mediates trans-repression of TLR4-induced cytokine expression; the function seems to require its sumoylation and prevents N-CoR nuclear receptor corepressor clearance from target genes such as IL1B and NOS2. Involved in the TLR9-mediated protective mechanism in intestinal inflammation. Plays an anti-inflammatory role in liver inflammation; proposed to inhibit proinflammatory (but not antiapoptotic) NF-kappa-B signaling.