EC Number   |
General Information |
Reference |
|---|
   2.8.2.4 | evolution |
gene structure and genomic organization of each cynomolgus SULTs are similar to those of the human orthologues. SULT1B1 and SULT1E1 form a gene cluster |
760542 |
| 2.8.2.4 | evolution |
the estrogen sulfotransferase (EST or SULT1E1) is a member of the sulfotransferase family. It shares high amino acid homology with other sulfotransferase isoforms. But EST is believed to have unique functions due to its distinct substrates and specific tissue distribution and sex-regulated expression. The effect of EST on adipogenesis seems to be species specific. The anti-adipogenic activity of EST in mice is opposite to the pro-adipogenic effect of the same enzyme in human adipocytes |
-, 760317 |
| 2.8.2.4 | malfunction |
ablation of the enzyme accelerates the differentiation of primary preadipocytes |
725979 |
| 2.8.2.4 | malfunction |
administration of low dose triclosan to pregnant ewes results in placental uptake and reduced estradiol sulfotransferase activity in fetal liver and placenta, effects of triclosan exposure (administered to late gestation fetal sheep for two days either by direct infusion into the fetal circulation or infusion into the maternal blood) of pregnant ewes on placental and hepatic sulfotransferase activity, overview. Placenta contained higher concentrations of triclosan than liver in each individual sheep in both treatment groups |
762495 |
| 2.8.2.4 | malfunction |
enzyme ablation sensitizes mice to sepsis-induced death |
739148 |
| 2.8.2.4 | malfunction |
EST ablation produces completely opposite metabolic phenotype in female and male obese mice. Male Est-/- mice develop age-dependent Leydig cell hypertrophy/hyperplasia and impaired steroidogenesis, have reduced total and forward sperm motility, and produce smaller litters compared with age-matched wild-type males. In female mice, ablation of the mouse Sult1e1 gene causes placental thrombosis and spontaneous fetal loss, which is associated with elevated free estrogen levels in the circulation and the amniotic fluid. The expression of EST can also be stimulated in the liver by dexamethasone through the activation of the glucocorticoid receptor (GR). The activation of GR can lead to hyperglycemia in genetically obese viable yellow (Avy) female mice due to an aberrant shift in hepatic androgen/ estrogen balance. Castration of male mice abolishes EST expression in the epididymal fat, whereas testosterone supplementation restores it. Although EST expression can be induced in the parametrial fat of female mice, whole body ablation of EST does not cause any differences in fat indices (fat weight normalized to body weight) between female WT and EST-/- mice. EST-/- male mice have their epididymal and inguinal fat indices significantly higher than those of the wild-type mice. Adipocyte size in EST-/- male mice is markedly larger than that of wild-type mice, but under chow diet, these changes are not accompanied by obvious metabolic abnormalities. EST loss in obese males worsens metabolic phenotype. Female obe mice exhibit completely opposite metabolic phenotypes. Whole body loss of EST expression in the ob/ob background decreases hepatic gluconeogenesis and lipogenesis, improves body composition and insulin sensitivity, and increases energy expenditure. Ablation of EST in female ob/ob mice does not affect WAT inflammation |
-, 760317 |
| 2.8.2.4 | malfunction |
impairment in the hepatic estrogen sulfotransferase (SULT1E1) protein expression are noticed with interfered hepatic free-thiols only in a N-ethyl-N-nitrosourea (ENU) and a xenograft-estradiol (E2) group compared to the arsenic group. Impairment of SULT1E1 expression and E2 regulations through oxidant-stress signalling. Oxidative stress has a vital role in E2 regulation and can structurally modify or alter the expression level of E2 metabolizing proteins. As such, estrogen receptors lose their DNA binding ability and thus impairing transcription. The estradiol binding site gets blocked in estrogen sulfotransferase under oxidative stress |
-, 761874 |
| 2.8.2.4 | malfunction |
inhibition of Eenzyme activity produces placental thrombosis and spontaneous abortion |
739665 |
| 2.8.2.4 | malfunction |
knock-down of the enzyme in HUVEC cells results in regulation of genes involved in inflammation and lipid metabolism |
725965 |
| 2.8.2.4 | malfunction |
loss of Est in male ob/ob mice, but not in female ob/ob mice, exacerbates the diabetic phenotype. Transgenic reconstitution of Est in the adipose tissue, but not in the liver, attenuates diabetic phenotype in Est-deficient ob/ob mice (obe mice). Mechanistically, adipose reconstitution of Est in obe mice (oae mice) results in reduced local and systemic inflammation, improved insulin sensitivity, and increased energy expenditure. At the molecular level, adipose induction of lipocalin-2 (Lcn2) in oae males may have contributed to the inhibition of inflammation because the level of Lcn2 is negatively associated with tumor necrosis factor (TNF) alpha expression, and treatment of differentiated adipocytes with Lcn2 antagonizes TNFalpha-responsive inhibition of insulin signaling. The metabolic benefit of adipose reconstitution of Est is sex specific, because adipose reconstitution of Est in obe females has little effect. Interestingly, despite their improved metabolic functions, obe male mice with reconstituted Est in their adipose tissue fail to ameliorate the impairment of the structure and function of the pancreatic islets |
-, 760988 |
