STS Antibody
Description
Definition and Function
The STS antibody is a polyclonal or monoclonal antibody designed to detect the STS enzyme (UniProt ID: P08842) in various biological samples . It binds specifically to the enzyme’s protein structure, enabling its detection in assays like Western blot (WB), immunohistochemistry (IHC), and immunofluorescence (IF) . The enzyme itself is expressed primarily in the liver, adrenal glands, and skin, where it facilitates the conversion of sulfated steroids into active forms .
Applications in Research
The STS antibody is employed in diverse research contexts:
Antibody Validation and Performance
The STS antibody’s performance has been rigorously validated:
Research Contributions
The STS antibody has advanced studies in steroid metabolism and disease:
Product Specs
Target Background
- Polymorphisms within the STS gene have been associated with attention-deficit/hyperactivity disorder. PMID: 28367959
- Elevated STS levels have been observed in preeclamptic placentas and maternal whole blood. Research suggests that STS might influence sFlt1 secretion by regulating sFlt1-i13 transcription, rather than through alterations in syncytialization. PMID: 27871476
- Studies indicate that STS plays a crucial role in steroid biosynthesis by regulating the availability of circulating cholesterol. PMID: 27531568
- In contrast to findings in boys with ADHD, the G-allele at rs17268988 of STS in healthy men has been linked to enhanced cognitive function. PMID: 28293481
- Overexpression of miR-661 sensitized tumors to TRAIL or STS-induced apoptosis in a xenograft mouse model. These effects were attenuated by co-expression of CYC1. PMID: 28391262
- Collectively, STS point mutations exhibit restricted localization, leading to efficient impairment of the corresponding enzyme activity. These mutations are less likely to be responsible for the phenotypic heterogeneity observed in XLRI subjects. PMID: 26387488
- STS expression was not significantly correlated with disease-free survival (DFS) or overall survival (OS), despite its positive expression in 27% of endometrial cancer patients. Therefore, the prognostic significance of STS in endometrial cancer remains unclear and requires further investigation. PMID: 26996578
- Induction of STS facilitates the conversion of inactive estrogen sulfates to active estrogens, which in turn attenuates NF-kappaB-mediated inflammation. PMID: 26220752
- The antagonistic actions of glucocorticoids and NFkB on STS expression resemble the regulation of inflammatory response proteins. PMID: 26631368
- A novel nonsense mutation in the STS gene has been reported in a patient with X-linked ichthyosis. PMID: 26421812
- Both estrogen sulfatase (STS) and estrogen sulfotransferase (EST) were found to be highly expressed in human umbilical vein endothelial cells (HUVECs). PMID: 26458420
- The influence of steroid hormones on estrogen sulfotransferase and steroid sulfatase expression has been investigated in endometriosis tissue and stromal cells. PMID: 26723541
- STS represents one of the primary pathways involved in regenerating biologically active steroids in both steroidogenic and nonsteroidogenic tissues. [Review] PMID: 26213785
- Analyses have revealed that two distinct phenotypes in a patient were attributed to independent genetic defects: a genomic rearrangement involving the Kallmann syndrome 1 gene and a point mutation in the steryl-sulfatase gene. PMID: 25726327
- An up-regulation of STS mRNA expression was observed in both arm and subumbilical skin biopsies of patients with idiopathic hirsutism. PMID: 26194504
- Genetic variations in ARSC may be associated with changes in mammographic density after women discontinue estrogen-progestin therapy. PMID: 25499601
- STS has been identified in human pre-osteoblastic bone cells and is believed to influence bone cell growth. PMID: 25042472
- Complete deletions in the STS gene have been reported in Pakistani families with X-linked ichthyosis. PMID: 24480088
- Findings suggest that steroid sulfatase expression may be down-regulated during the process of large intestinal carcinogenesis. PMID: 23916543
- Data indicate that the expression of STS and 17beta-hydroxysteroid dehydrogenase isoenzymes is up-regulated in subcutaneous abdominal fat of morbidly obese women compared to morbidly obese men. PMID: 24081738
- A microdeletion within Xp22.3 containing STS, identified using array comparative genomic hybridization (aCGH), in an individual with suspected pre-Descemet corneal dystrophy and X-linked ichthyosis highlights the clinical utility of copy number variation analysis. PMID: 23807007
- IGF-II induces steroid sulfatase expression via a PI3-kinase/Akt-NF-kappaB signaling pathway in PC-3 cells. This induction may contribute to estrogen production and estrogen-mediated carcinogenesis. PMID: 24055520
- Genetic variants in SULT2A1, PAPSS2, and STS are not considered predisposing factors for polycystic ovary syndrome. PMID: 23861462
- No significant difference in placental activity was observed between women with polycystic ovarian syndrome and control subjects. PMID: 23122578
- Genetic variations affecting steroid sulfatase expression or activity might influence the function of brain regions implicated in attention deficit hyperactivity disorder (ADHD). PMID: 21255266
- Filaggrin defects can synergize with steroid sulfatase deficiency to exacerbate the ichthyosis phenotype. PMID: 21945601
- Recent research findings on STS and EST in various estrogen-dependent carcinomas are summarized. PMID: 21073915
- This comprehensive review focuses on recent advancements in steroid sulfatase research. PMID: 21693170
- A novel point mutation in the STS gene has been reported in a patient with X-linked recessive ichthyosis. PMID: 21530180
- Genetic variations in the STS gene may contribute to ADHD susceptibility, and one polymorphism has been associated with lower STS mRNA expression and a higher prevalence in female ADHD homozygotes. PMID: 20862695
- X-linked recessive ichthyosis is caused by a deficiency in steroid sulfatase (STS), whose gene has been mapped to the X chromosome. PMID: 20236202
- Six novel single nucleotide polymorphisms (SNPs) in the steroid sulfatase gene have been identified in a Japanese population. PMID: 20814163
- A significant increase in STS levels was observed following exemestane neoadjuvant therapy of postmenopausal ER-positive breast carcinoma. This may represent a compensatory response of breast carcinoma tissues to estrogen depletion. PMID: 20151319
- Mutations in both steroid sulfatase and filaggrin have been implicated in X-linked ichthyosis. PMID: 20149601
- Analysis of deletions suggests a complex origin, beyond homologous recombination, of deletion mutants. PMID: 11844872
- In the human hair follicle, STS is concentrated in the dermal papilla. PMID: 11886493
- Regulation of estrogen activity in human endometrium: the effect of IL-1beta on steroid sulfatase activity in human endometrial stromal cells. PMID: 11996939
- Data demonstrate that LNCaP prostate cancer cells contain a steryl sulfatase with properties similar to that found in human breast cancer cells. PMID: 12231117
- The structure of STS, purified from the microsomal fraction of human placentas, has been determined by X-ray crystallography. PMID: 12657638
- Levels of STS and estrogen sulfotransferase mRNA and activity may be significantly associated with the degree of atherosclerotic changes in female aorta. This association may be related to cytokines produced in situ, such as IL-1beta, in human atherosclerotic lesions. PMID: 14507642
- Estrogen-dependent cell growth of the estrogen sulfatase-transfected cell clones was found to be abolished due to the enhanced sulfoconjugation of estrogen. PMID: 14556660
- Steroid sulfatase increases steroid acute regulatory protein expression levels and stimulates steroid production. PMID: 14969586
- SSase is concentrated in lamellar bodies (LB), and secreted into the stratum corneum (SC) interstices, along with other LB-derived lipid hydrolases. There, it degrades CSO4, generating some cholesterol for the barrier. PMID: 15009711
- Strong activity and mRNA expression of DHEAS desulfating STS were found, twice as high in cerebral neocortex than in subcortical white matter. Cerebral STS resembled the characteristics of the known placental enzyme. PMID: 15056284
- Dehydroepiandrosterone blood levels are influenced by a steroid sulfatase polymorphism following acute resistance exercise. PMID: 15152080
- Gonadotropin-releasing hormone agonist (leuprolide) inhibits estrone sulfatase expression in cystic endometriosis in the ovary. PMID: 15302278
- Increased steroid sulfatase expression is associated with estrogen-dependent endometrial carcinomas. PMID: 15355916
- Findings of steroid sulfatase localized in the cytoplasm of the cumulus cells and expression of STS mRNA suggest a local steroidal regulation mechanism in cumulus cells. PMID: 16084891
- Studies on the localization of steroid sulfatase have been conducted. PMID: 16399357
- Corticotrophin-releasing hormone (CRH) increased, whereas alpha-helical CRH decreased, the mRNA levels of STS, CYP19A1, and HSD17B1, the key enzymes for estrogen synthesis. PMID: 16467490
Q&A
What is the role of STS antibodies in molecular biology research?
Steroid sulfatase (STS) antibodies are essential tools for investigating the enzymatic activity and biological functions of steroid sulfatase, a key enzyme involved in the hydrolysis of sulfated steroid hormones such as cholesterol sulfate. In molecular biology, STS antibodies are used to detect the presence and quantify the expression of STS protein in various tissues and cell types through techniques like Western blotting (WB), immunohistochemistry (IHC), and immunofluorescence (IF). These antibodies enable researchers to study the enzyme's role in steroid metabolism, cellular signaling pathways, and its implications in diseases such as cancer and X-linked ichthyosis (XLI) . For example, immunohistochemical analysis has revealed STS expression patterns in human tissues like placenta, skin, and kidney . Additionally, recombinant antigens used in these antibodies reduce nonspecific reactions, enhancing sensitivity .
How can STS antibodies be utilized to study disease mechanisms?
STS antibodies are instrumental in exploring disease mechanisms where steroid metabolism plays a critical role. For instance, STS overexpression has been linked to breast cancer subtypes with improved prognosis due to enhanced intratumoral estrogen metabolism . Conversely, STS deficiency can lead to cellular senescence through cholesterol sulfate accumulation and altered gene expression profiles such as YPEL3 induction . These antibodies allow researchers to trace enzymatic activity changes associated with disease progression or therapeutic interventions. Furthermore, STS inhibition has been studied as a potential therapeutic strategy for aging-related diseases like Alzheimer's by modulating sulfated steroid hormone levels .
What experimental controls are necessary when using STS antibodies?
Proper experimental design necessitates rigorous controls to ensure data reliability when using STS antibodies. Controls include unstained samples to establish baseline fluorescence levels in flow cytometry experiments or isotype controls to rule out nonspecific binding of secondary antibodies . Compensation controls are vital for multicolor flow cytometry experiments to correct spectral overlap between fluorophores. For Western blotting or IHC applications, researchers should include positive controls (e.g., tissues known to express STS) and negative controls (e.g., tissues lacking STS expression or samples treated with blocking peptides). These measures help validate antibody specificity and minimize artifacts.
How do researchers address false positives or negatives in STS antibody assays?
False positives or negatives can arise due to cross-reactivity with other molecules or technical errors during assay execution. For example, biological false positives may occur due to conditions like autoimmune diseases or viral infections . To mitigate these issues, researchers employ highly purified native antigens or recombinant antigens that reduce nonspecific reactions . Dilution protocols can also address false negatives caused by the prozone phenomenon—a scenario where antigen-antibody ratios exceed optimal levels . Advanced statistical models like finite mixture models based on skew-normal distributions can classify serological data more accurately by accounting for asymmetry in antibody-positive versus antibody-negative populations .
How can computational models enhance the design of STS-specific antibodies?
Computational modeling has revolutionized antibody design by predicting specificity profiles based on biophysical principles and experimental data. For STS-specific antibodies, researchers use phage display libraries combined with high-throughput sequencing to select variants with desired binding properties . These models optimize energy functions associated with ligand interactions to create either cross-specific or highly specific antibody sequences . Such approaches minimize experimental biases and enable the generation of novel sequences not present in initial libraries.
What are the challenges associated with interpreting serological data for STS?
Interpreting serological data for STS involves addressing variability among laboratory protocols and technician expertise. Manual tests like nontreponemal assays require subjective interpretation of titers relative to syphilis stages . Automated treponemal immunoassays offer higher throughput but must be integrated into diagnostic algorithms alongside manual tests for comprehensive analysis . Statistical tools such as finite mixture models provide robust frameworks for analyzing serological data by fitting distributions that account for skewness observed in antibody-positive populations .
What methods are available for quantifying STS activity?
Quantifying STS activity typically involves enzymatic assays that measure hydrolysis rates of sulfated substrates like cholesterol sulfate under controlled conditions . Immunoassays such as enzyme-linked immunosorbent assays (ELISA) provide quantitative measurements of STS protein levels using specific antibodies . High-throughput systems like HISCL-2000i automate TP-Ab testing for rapid analysis while maintaining sensitivity and reproducibility .
How does aging research benefit from studying steroid sulfatase?
Aging research has uncovered links between steroid sulfatase activity and longevity regulation. In Caenorhabditis elegans, loss-of-function mutations in the steroid sulfatase gene (sul-2) increase lifespan by elevating sulfated steroid hormones that modulate longevity pathways involving insulin-like growth factors and TGF-β signaling . Pharmacological inhibition of STS using compounds like STX64 replicates these effects in mammalian models, suggesting potential applications for aging-related diseases such as Alzheimer's disease.
How do advanced imaging techniques contribute to studying STS localization?
Advanced imaging techniques like confocal microscopy enable precise localization of STS within cellular compartments using fluorescently labeled antibodies . Immunofluorescence assays have demonstrated cytosolic versus nuclear distribution patterns influenced by cholesterol sulfate treatment in keratinocytes . Such localization studies provide insights into the enzyme's functional roles within specific signaling pathways.
