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 and nucleus. Predicted to be part of RNA polymerase II transcription regulator complex. 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], 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', 5'-AMP results in increased export of Cholesterol]]
morroniside inhibits the reaction [Glucose results in decreased expression of NR1H2 mRNA], 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, [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], 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, [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], 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], 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, [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, [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, [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 nefazodone] results in increased expression of NR1H2 mRNA
Vecuronium Bromide inhibits the reaction [Nicotine results in decreased expression of NR1H2 mRNA], 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], [Dust results in increased abundance of 2-ethylhexyldiphenylphosphate] inhibits the reaction [T0901317 results in increased activity of NR1H2 protein]
[homocastasterone analog co-treated with Streptozocin] results in increased expression of NR1H2 mRNA, 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], 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], 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], 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).
Heterodimeric interaction between retinoid X receptor alpha and orphan nuclear receptor OR1 reveals dimerization-induced activation as a novel mechanism of nuclear receptor activation.
