Application | Comment | Organism |
---|---|---|
medicine | the HNF4alpha-SULT2B1b-CS axis represents a key endogenous mechanism to prevent uncontrolled gluconeogenesis. Thiocholesterol may be used as a therapeutic agent to manage hyperglycemia | Homo sapiens |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
cytosol | - |
Homo sapiens | 5829 | - |
cytosol | - |
Mus musculus | 5829 | - |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
3'-phosphoadenylyl sulfate + cholesterol | Homo sapiens | - |
adenosine 3',5'-bisphosphate + cholesterol 3-sulfate | - |
? | |
3'-phosphoadenylyl sulfate + cholesterol | Mus musculus | - |
adenosine 3',5'-bisphosphate + cholesterol 3-sulfate | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | O00204 | - |
- |
Mus musculus | O35400 | - |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
Hep-G2 cell | - |
Homo sapiens | - |
hepatocyte | - |
Homo sapiens | - |
hepatocyte | - |
Mus musculus | - |
liver | - |
Homo sapiens | - |
liver | - |
Mus musculus | - |
primary cell | - |
Homo sapiens | - |
primary cell | - |
Mus musculus | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
3'-phosphoadenylyl sulfate + cholesterol | - |
Homo sapiens | adenosine 3',5'-bisphosphate + cholesterol 3-sulfate | - |
? | |
3'-phosphoadenylyl sulfate + cholesterol | - |
Mus musculus | adenosine 3',5'-bisphosphate + cholesterol 3-sulfate | - |
? |
Synonyms | Comment | Organism |
---|---|---|
cholesterol sulfotransferase | - |
Homo sapiens |
cholesterol sulfotransferase | - |
Mus musculus |
SULT2B1b | - |
Homo sapiens |
SULT2B1b | - |
Mus musculus |
Organism | Comment | Expression |
---|---|---|
Homo sapiens | the basal expression levels of SULT2B1b and G6Pase ae decreased in human primary epatocytes treated with the HNF4alpha inhibitor BIM5078 | down |
Homo sapiens | HNF4alpha induces the expression of SULT2B1b in human liver cells. In the human hepatoma HepG2 cells, transfection with the HNF4alpha expression vector increases the expression of SULT2B1b. In human primary hepatocytes (HPH), treatment of cells with the HNF4alpha activator linoleic acid induces the expression of both SULT2B1b | up |
Mus musculus | HNF4alpha positively regulates the expression of Sult2B1b in mouse primary hepatocytes and in mouse liver, expression of Sult2B1b is induced by HNF4alpha upon fasting | up |
General Information | Comment | Organism |
---|---|---|
malfunction | downregulation or ablation of Sult2B1b enhances the gluconeogenic activity of HNF4alpha, which may cause increased acetylation of HNF4alpha as a result of decreased expression of the HNF4alpha deacetylase sirtuin 1 (Sirt1). Sult2B1b-/- mice exhibit elevated fasting blood glucose levels. Thiocholesterol is a hydrolysis-resistant derivative of cholesterol, which shows superior activity to that of the native cholesterol in inhibiting gluconeogenesis and improving insulin sensitivity in high-fat-diet-induced diabetic mice | Mus musculus |
metabolism | regulation of cholesterol sulfotransferase SULT2B1b by hepatocyte nuclear factor 4alpha constitutes a negative feedback control of hepatic gluconeogenesis. The SULT2B1b gene is a transcriptional target of HNF4alpha | Homo sapiens |
metabolism | regulation of cholesterol sulfotransferase SULT2B1b by hepatocyte nuclear factor 4alpha constitutes a negative feedback control of hepatic gluconeogenesis. The SULT2B1b gene is a transcriptional target of HNF4alpha. Recruitment of HNF4alpha to the mouse Sult2B1b gene promoter is confirmed by chromatin immunoprecipitation assay on mouse primary hepatocytes | Mus musculus |
physiological function | sulfotransferases (SULTs) catalyze the transfer of a sulfate group from 3'-phosphoadenosine 5'-phosphosulfate (PAPS) to an acceptor molecule. Sulfation plays an essential role in regulating the chemical and functional homeostasis of endogenous and exogenous molecules. The cholesterol sulfotransferase SULT2B1b preferentially catalyzes the sulfoconjugation of cholesterol to synthesize cholesterol sulfate. SULT2B1b inhibits hepatic gluconeogenesis by antagonizing the gluconeogenic activity of hepatocyte nuclear factor 4alpha (HNF4alpha). Regulation of cholesterol sulfotransferase SULT2B1b by hepatocyte nuclear factor 4alpha constitutes a negative feedback control of hepatic gluconeogenesis. SULT2B1b also plays a restrictive role in HNF4alpha-mediated fasting-responsive gluconeogenesis | Homo sapiens |
physiological function | sulfotransferases (SULTs) catalyze the transfer of a sulfate group from 3'-phosphoadenosine 5'-phosphosulfate (PAPS) to an acceptor molecule. Sulfation plays an essential role in regulating the chemical and functional homeostasis of endogenous and exogenous molecules. The cholesterol sulfotransferase SULT2B1b preferentially catalyzes the sulfoconjugation of cholesterol to synthesize cholesterol sulfate. SULT2B1b inhibits hepatic gluconeogenesis by antagonizing the gluconeogenic activity of hepatocyte nuclear factor 4alpha (HNF4alpha). Regulation of cholesterol sulfotransferase SULT2B1b by hepatocyte nuclear factor 4alpha constitutes a negative feedback control of hepatic gluconeogenesis. SULT2B1b also plays a restrictive role in HNF4alpha-mediated fasting-responsive gluconeogenesis | Mus musculus |