SULT1A1 Lysate
- Known as:
- SULT1A1 Lysate
- Catalog number:
- NBL1-16601
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SULT1A1 Lysate
Related genes to: SULT1A1 Lysate
- Gene:
- SULT1A1 NIH gene
- Name:
- sulfotransferase family 1A member 1
- Previous symbol:
- STP, STP1
- Synonyms:
- P-PST
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-08-23
- Date modifiied:
- 2016-10-05
Related products to: SULT1A1 Lysate
Related articles to: SULT1A1 Lysate
- Phenyl sulfate (PS), a gut microbiota-derived metabolite implicated in the pathogenesis of diabetic kidney disease, is generated through microbial conversion of dietary tyrosine to phenol, followed by hepatic sulfation via SULT1A1. We developed an oral tyrosine challenge test (OTyCT) to phenotype individual PS-producing capacity. Forty-eight healthy adults underwent a standardized tyrosine load with serial plasma PS levels measured over 48 h using LC-MS. OTyCT revealed substantial interindividual variability of PS production independent of baseline PS levels, highlighting marked heterogeneity in host-microbiome metabolic interactions. Sixteen participants in the highest tertile of the incremental area under the curve of PS were defined as high-PS producers. High PS producers exhibited distinct gut microbial signatures despite comparable abundances of known phenol-biosynthetic genes and host SULT1A1 genotypes. These findings suggest that susceptibility to PS-related complications may vary according to gut microbial profiles, supporting OTyCT as a practical tool for metabolic phenotyping and microbiome-informed precision nutrition. Clinical Trial registry name and registration number: Identification of P-Cresyl Sulfate Producer Phenotype by Oral Tyrosine Challenge Test: Interactions Among Diet, Gut Microbiota, and Host Genome, NCT04204174. - Source: PubMed
Publication date: 2026/06/02
Lin Ting-YunHung Szu-ChunAbe Takaaki - Chronic spontaneous urticaria (CSU) is a histamine-mediated inflammatory skin disease, but key inflammatory proteins remain undefined. - Source: PubMed
Publication date: 2026/04/17
Chen JialuYao YuxuDeng LijunChen LuLu ZhenzhongJi JiangJiao Qingqing - Sulfate is a vital nutrient for healthy brain development. More than 90 sulfate-related genes are highly conserved across mammalian species, with 16 of these genes being clinically reportable for adverse brain conditions. To determine the potential involvement of additional sulfate-related genes in human neuropathology, this study curated the spatial and temporal expression patterns of all known sulfate biology genes in the human fetal brain from 8 to 37 post conception weeks (pcw) using data from the BrainSpan database and performed network analysis to cluster sulfate-related genes with genes involved in neurodevelopmental processes. A total of 64 sulfate-related genes were abundantly or moderately expressed in 11 brain regions throughout gestation. Steady state expression was observed for some of these genes from 8 to 37 pcw, including genes that encode sulfotransferases (, ), sulfatases (, , , ), sulfatase modifying enzyme (), key enzymes in amino acid metabolism (, ), sulfate transporter (), as well as genes involved in neurodevelopmental processes (, , , , , ). Between 21-24 weeks, there were numerous clusters of sulfate biology genes with neurodevelopmental genes involved in neuronal migration ( and synaptogenesis (, , , ). At 8-13 and 17-21 pcw, fifteen sulfate genes (, , , , , , , , , , , , , , ) were expressed in the hippocampus and clustered with genes involved in neurogenesis, differentiation and synaptogenesis (, , ). Overall, this study identified 48 sulfate-related genes with moderate/abundant expression in the fetal brain that are coexpressed with genes for neurodevelopmental processes but are not considered in clinical settings. These findings provide information for future studies into the physiological roles of sulfate-related genes that are expressed in the fetal brain. - Source: PubMed
Publication date: 2026/05/08
Vijayakumar PrasidheeSummers Kim MDawson Paul A - : Tamoxifen is widely used in the treatment of hormone receptor-positive breast cancer and has been shown to successfully reduce recurrence and mortality rates. Nonetheless, variability in patient response to tamoxifen treatment is observed with up to 40% of patients experiencing recurrence. Genetic polymorphisms in pharmacogenes encoding enzymes involved in tamoxifen metabolism have been linked to some of this observed interindividual variability. The pharmacogenetics of tamoxifen in populations of African descent remain understudied, creating difficulties in pinpointing the primary factors behind the observed variable response. To address this gap, this study aimed to investigate the role of genetic variation in tamoxifen treatment outcomes in a South African cohort. : Participants included 166 Mixed and African Ancestry breast cancer patients who had received tamoxifen treatment. Genetic characterization was performed for 53 single nucleotide polymorphisms (SNPs) and two copy number variations across eight drug-metabolizing enzymes, including cytochrome P450s (, , , ), UDP-glucuronosyltransferases (), and sulfotransferases (, , ). The association between genotypes and disease-free survival (DFS) was evaluated using Cox proportional hazards regression models. : The or * genotype showed a nominal association with improved DFS ( = 0.049), with a similar trend observed for rs11888492. In contrast, rs3775779 heterozygosity showed a nominal association with reduced DFS ( = 0.044). SNPs (rs4149393, rs4149394, rs1042157) demonstrated trends toward reduced DFS. : These exploratory findings highlight the need for more inclusive pharmacogenomic research and point to potential biomarkers for optimizing tamoxifen therapy in African populations. - Source: PubMed
Publication date: 2026/03/31
Kruger BiancaChimusa Emile RAbera Aron BSingh JesmikaShamley DelvaDandara Collet - Estragole (ES) is a phenylpropene naturally occurring in various herbs and spices, such as fennel and basil. Humans are exposed to ES via the diet or herbal medicinal products. Following its gastrointestinal resorption, hepatic bioactivation of ES by Cytochrome P450 monooxygenases (CYPs) and sulfotransferases (SULTs) can lead to DNA adduct formation and liver cancer in rodents. Up to now, no data is available on ES-dependent DNA adducts in human tissue, which would however be important for human risk assessment. Our work thus analyzed whether ES-derived DNA adducts are present in human liver samples. Furthermore, DNA adduct formation after repetitive ES exposure and upon incubation with an ES-containing bitter fennel infusion was studied in human liver cells. Using a sensitive UHPLC-MS/MS method, we detected E3'-N-dG adducts in a multitude of human liver samples. The adduct levels correlated positively with SULT1A1, but not CYP1A2 protein expression. Noteworthy, the E3'-N-dA adduct was not found in the analyzed human liver tissue. Further experiments revealed that E3'-N-dG adducts accumulate in metabolically competent human liver cells after repetitive short-term exposure to ES, whereas the E3'-N-dA adduct was not detected at all. Finally, we provided evidence that ES from a bitter fennel tea preparation induces E3'-N-dG adducts in human liver cells, however at lower levels than expected. Altogether, this study demonstrated the occurrence of ES-derived DNA adducts in human liver tissue at levels comparable to the structurally related methyleugenol. Notably, the found DNA adduct levels are well below those reported to cause mutagenicity and clastogenicity in human cells and rodent in vivo models. - Source: PubMed
Publication date: 2026/03/31
Ackermann GAbel-Beckmann MQuarz CHalaczkiewicz MStegmüller SRichling EManolikakes GChristmann MKüpper J HSchrenk DFahrer J