Enables DNA-binding transcription activator activity, RNA polymerase II-specific; RNA polymerase II cis-regulatory region sequence-specific DNA binding activity; and nuclear retinoid X receptor binding activity. Contributes to sequence-specific DNA binding activity. Involved in regulation of gene expression; response to nutrient levels; and retinoic acid receptor signaling pathway. Predicted to be located in cytoplasm. Predicted to be part of RNA polymerase II transcription regulator complex. Predicted to be active in nucleus. Biomarker of obesity. Human ortholog(s) of this gene implicated in obesity and type 2 diabetes mellitus. Orthologous to human NR1H2 (nuclear receptor subfamily 1 group H member 2); INTERACTS WITH (S)-nicotine; 2,3,7,8-tetrachlorodibenzodioxine; 2,4-dinitrotoluene.
Vecuronium Bromide inhibits the reaction [Nicotine results in decreased expression of NR1H2 mRNA] and Vecuronium Bromide inhibits the reaction [Nicotine results in decreased expression of NR1H2 protein]
NR1H2 gene mutant form inhibits the reaction [pitavastatin inhibits the reaction [8-((4-chlorophenyl)thio)cyclic-3' and 5'-AMP results in increased export of Cholesterol]]
morroniside inhibits the reaction [Glucose results in decreased expression of NR1H2 mRNA] and morroniside inhibits the reaction [Glucose results in decreased expression of NR1H2 protein]
[[sodium arsenite results in increased abundance of Arsenic] co-treated with [manganese chloride results in increased abundance of Manganese]] results in increased expression of NR1H2 mRNA
[[sodium arsenite results in increased abundance of Arsenic] co-treated with [manganese chloride results in increased abundance of Manganese]] results in increased expression of NR1H2 mRNA
[Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Cyclosporine] results in increased expression of NR1H2 mRNA and [Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with nefazodone] results in increased expression of NR1H2 mRNA
[Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Cyclosporine] results in increased expression of NR1H2 mRNA
morroniside inhibits the reaction [Glucose results in decreased expression of NR1H2 mRNA] and morroniside inhibits the reaction [Glucose results in decreased expression of NR1H2 protein]
[Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Cyclosporine] results in increased expression of NR1H2 mRNA and [Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with nefazodone] results in increased expression of NR1H2 mRNA
Etoposide promotes the reaction [NR1H2 protein results in increased expression of CETP mRNA] and NR1H2 mutant form inhibits the reaction [Etoposide results in increased expression of CETP mRNA]
morroniside inhibits the reaction [Glucose results in decreased expression of NR1H2 mRNA] and morroniside inhibits the reaction [Glucose results in decreased expression of NR1H2 protein]
[Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Cyclosporine] results in increased expression of NR1H2 mRNA and [Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with nefazodone] results in increased expression of NR1H2 mRNA
[Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Cyclosporine] results in increased expression of NR1H2 mRNA and [Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with nefazodone] results in increased expression of NR1H2 mRNA
[Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Cyclosporine] results in increased expression of NR1H2 mRNA and [Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with nefazodone] results in increased expression of NR1H2 mRNA
[[sodium arsenite results in increased abundance of Arsenic] co-treated with [manganese chloride results in increased abundance of Manganese]] results in increased expression of NR1H2 mRNA
[[sodium arsenite results in increased abundance of Arsenic] co-treated with [manganese chloride results in increased abundance of Manganese]] results in increased expression of NR1H2 mRNA
[[sodium arsenite results in increased abundance of Arsenic] co-treated with [manganese chloride results in increased abundance of Manganese]] results in increased expression of NR1H2 mRNA
[Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with nefazodone] results in increased expression of NR1H2 mRNA
Vecuronium Bromide inhibits the reaction [Nicotine results in decreased expression of NR1H2 mRNA] and Vecuronium Bromide inhibits the reaction [Nicotine results in decreased expression of NR1H2 protein]
2-ethylhexyldiphenylphosphate inhibits the reaction [T0901317 results in increased activity of NR1H2 protein] and [Dust results in increased abundance of 2-ethylhexyldiphenylphosphate] inhibits the reaction [T0901317 results in increased activity of NR1H2 protein]
[perfluorooctane sulfonic acid co-treated with Cellulose] results in decreased expression of NR1H2 mRNA and [perfluorooctane sulfonic acid co-treated with Pectins] results in decreased expression of NR1H2 mRNA
[[sodium arsenite results in increased abundance of Arsenic] co-treated with [manganese chloride results in increased abundance of Manganese]] results in increased expression of NR1H2 mRNA
[homocastasterone analog co-treated with Streptozocin] results in increased expression of NR1H2 mRNA and homocastasterone analog inhibits the reaction [Streptozocin results in decreased expression of NR1H2 protein]
NR1H2 mutant form inhibits the reaction [Teniposide results in increased expression of CETP mRNA] and Teniposide promotes the reaction [NR1H2 protein results in increased expression of CETP mRNA]
[Dust results in increased abundance of triphenyl phosphate] inhibits the reaction [T0901317 results in increased activity of NR1H2 protein] and triphenyl phosphate inhibits the reaction [T0901317 results in increased activity of NR1H2 protein]
Vecuronium Bromide inhibits the reaction [Nicotine results in decreased expression of NR1H2 mRNA] and Vecuronium Bromide inhibits the reaction [Nicotine results in decreased expression of NR1H2 protein]
Suggestive evidence of associations between liver X receptor ß polymorphisms with type 2 diabetes mellitus and obesity in three cohort studies: HUNT2 (Norway), MONICA (France) and HELENA (Europe).
(-)-Epigallocatechin-3-Gallate Ameliorates Atherosclerosis and Modulates Hepatic Lipid Metabolic Gene Expression in Apolipoprotein E Knockout Mice: Involvement of TTC39B.
Heterodimeric interaction between retinoid X receptor alpha and orphan nuclear receptor OR1 reveals dimerization-induced activation as a novel mechanism of nuclear receptor activation.
Dingxin Recipe IV attenuates atherosclerosis by regulating lipid metabolism through LXR-α/SREBP1 pathway and modulating the gut microbiota in ApoE-/- mice fed with HFD.
