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The IV phenotype was exacerbated by co-inheritance of STS and FLG mutations in a Chinese family with ichthyosis.
Results revealed an essential role of the adipose STS in energy homeostasis in sex- and sex hormone-dependent manner. The metabolic harm of the STS transgene in male mice appeared to have resulted from increased androgen activity in the adipose tissue. The metabolic benefit of the STS transgene in female mice was accounted for by increased estrogenic activity in the adipose tissue.
CYP19A1 mRNA levels were lower in endometrial cancer (EC) than in controls. A novel highly sensitive and accurate protocol to assess SULT1E1 activity is presented. STS enzyme activity and the STS:SULT1E1 activity ratio seem to be lower in ECs than in controls. STS is an important route for estrogen supply in endometrial cells.
Polymorphisms of STS gene is associated with attention-deficit/hyperactivity disorder.
STS is increased in preeclamptic placentas and maternal whole blood. Our data suggests that STS may affect sFlt1 secretion by regulating sFlt1-i13 transcription, and not via alterations in syncytialisation.
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-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.
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 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-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.
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
represents one of the major pathways in regenerating biologically active steroids in both steroidogenic and nonsteroidogenic tissues [review]
Our analyses show that the two phenotypes in our patient are due to independent genetic defects: a genomic rearrangement involving the Kallmann syndrome 1 gene and a point mutation of the steryl-sulfatase gene.
In both arm and subumbilical skin biopsy of patients with idiopathic hirsutism, there was an up-regulation of STS mRNA expression.
Genetic variation in ARSC may be associated with change in mammographic density after women stop using estrogen-progestin therapy.
STS is present in human pre-osteoblastic bone cells and that it can influence bone cell growth
Data show the gene expression profiling of ABC transporters in seven tissues.
shows a high sequence identity (60%) to human ABCG2 gene and ABCG2 expression was 6-fold higher than ABCC2 and almost 42 fold higher than ABCB1, indicating that the ABCG2 probably plays a significant role in the disposition and excretion of xenobiotics
Results revealed an essential role of the adipose STS in energy homeostasis in sex- and sex hormone-dependent manner. Adipose expression of Sts was induced in the high-fat diet (HFD) and ob/ob models of obesity and type 2 diabetes.
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
Steroid sulfatase expression in the ovaries of the cyclic cows.
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).
, estrone sulfatase
, steryl-sulfate sulfohydrolase
, breast cancer resistance protein
, steroid sulfatase (microsomal), arylsulfatase C, isozyme S
, steroid sulphatase
, steroid sulfatase (microsomal), isozyme S