Enhancer ID: | E_01_0501 |
Species: | human |
Position : | chr12:100470925-100472925 |
Biosample name: | |
Experiment class : | High+Lowthroughput |
Enhancer type: | Enhancer |
Disease: | Non alcoholic fatty liver disease (nafld), inflammation |
Pubmed ID: | 29743187 |
Enhancer experiment: | Migration assay,Transient transfection,gene expression analysis,immunostaining, |
Enhancer experiment description: | In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases. |
Target gene : | LTB |
Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
Less strong evidence: | RNA-Seq |
Target gene experiment description: | In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases.;In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases. |
TF name : | NR1H4 |
TF experiment: | Migration assay,Transient transfection,gene expression analysis,immunostaining, |
TF experiment description: | In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases.;In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases. |
Enhancer function : | In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases. |
Enhancer function experiment: | Immunohistochemical staining |
Enhancer function experiment description: |
In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases. |
SNP ID: | -- |
GeneName | Pathway Name | Source | Gene Number |
---|---|---|---|
NR1H4 | Endogenous sterols | reactome | 22 |
NR1H4 | Nuclear Receptor transcription pathway | reactome | 51 |
NR1H4 | PPARA activates gene expression | reactome | 113 |
NR1H4 | Recycling of bile acids and salts | reactome | 15 |
NR1H4 | RXR and RAR heterodimerization with other nuclear receptor | pid | 26 |
NR1H4 | Synthesis of bile acids and bile salts | reactome | 7 |
NR1H4 | Synthesis of bile acids and bile salts via 27-hydroxycholesterol | reactome | 15 |
NR1H4 | Synthesis of bile acids and bile salts via 7alpha-hydroxycholesterol | reactome | 24 |
NR1H4 | Hs_Drug_Induction_of_Bile_Acid_Pathway_WP2289_88593 | wikipathways | 9 |