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Data show the gene expression profiling of ABC (show ABCB6 ELISA Kits) transporters in seven tissues.
shows a high sequence identity (60%) to human ABCG2 gene and ABCG2 expression was 6-fold higher than ABCC2 (show ABCC2 ELISA Kits) and almost 42 fold higher than ABCB1 (show ABCB1 ELISA Kits), indicating that the ABCG2 probably plays a significant role in the disposition and excretion of xenobiotics
Overexpression of STS in the liver improved metabolic functions in mouse models of obesity and type 2 diabetes through sex-specific mechanisms.
These data suggest that inactivating mutations and functional variants within STS might exert their influence on ADHD vulnerability, and disorder endophenotypes through modulation of the serotonergic system.
steroid sulfatase may influence core and associated ADHD behavioural endophenotypes via both developmental and ongoing mechanisms, and that the 39,X(Y*)O model may represent a useful tool for elucidating the neurobiological basis of these endophenotypes.
analysis of brain pathways mediating the pro-aggressive effect of the steroid sulfatase (Sts) gene
Our data suggest that variation within STS may be particularly associated with the inattentive subtype of ADHD
This study reveals that STS is a key player of steroid biosynthesis regulating the availability of circulating cholesterol.
In contrast to the situation in boys with ADHD, in healthy men, the G-allele at rs17268988 of STS is associated with enhanced cognition.
miR (show MLXIP ELISA Kits)-661 overexpression sensitized tumors to TRAIL or STS induced apoptosis in a xenograft mouse model, and these effects were attenuated by co-expression of CYC1 (show CYC1 ELISA Kits).
Collectively, STS point mutations demonstrate restricted localization, causing efficient impairment of the corresponding enzyme activity, and are more unlikely to be responsible for the phenotypic heterogeneity in XLRI subjects
STS expression was not significantly associated with DFS (show FST ELISA Kits) and OS, despite positive STS expression in 27% of endometrial cancer patients. Therefore, the role of STS as a prognostic factor in patients with endometrial cancer remains unclear and requires further research.
The induced STS facilitates the conversion of inactive estrogen sulfates to active estrogens, which in return attenuates the NF-kappaB (show NFKB1 ELISA Kits)-mediated inflammation.
The antagonistic actions of glucocorticoids and NFkB on STS expression are similar to the regulation of inflammatory response proteins
Letter/Case Report: novel nonsense mutation in the STS gene in X-linked ichthyosis (show LBR ELISA Kits).
Data show that both estrogen sulfatase (STS) and estrogen sulfotransferase (EST) were highly expressed in the human umbilical vein endothelial cells (HUVECs).
Effects of steroid hormone on estrogen sulfotransferase and on steroid sulfatase expression in endometriosis tissue and stromal cells
These results suggest that the availability of estrogens in the boar epididymis may be locally controlled also by steroid sulphatase and estrogen sulphotransferase.
The protein encoded by this gene catalyzes the conversion of sulfated steroid precursors to estrogens during pregnancy. The encoded protein is found in the endoplasmic reticulum, where it acts as a homodimer. Mutations in this gene are known to cause X-linked ichthyosis (XLI).
steroid sulfatase (microsomal), arylsulfatase C, isozyme S
, breast cancer resistance protein
, arylsulfatase C
, steryl-sulfate sulfohydrolase
, estrone sulfatase
, steroid sulphatase