Mouse polyclonal to SULT1A1, Host Mouse
- Known as:
- Mouse pab SULT1A1, Host Mouse
- Catalog number:
- YF-PA14863
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal SULT1A1 Host
Related genes to: Mouse polyclonal to SULT1A1, Host Mouse
- 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: Mouse polyclonal to SULT1A1, Host Mouse
Related articles to: Mouse polyclonal to SULT1A1, Host Mouse
- : 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 - : Tamoxifen remains the cornerstone of endocrine therapy for hormone receptor-positive breast cancer across Africa. Understanding the factors that influence tamoxifen tolerability is critical, as treatment-related side effects can reduce adherence and compromise therapeutic outcomes. Yet, the contribution of pharmacogenetic variation to tamoxifen-related toxicity remains poorly characterized in African populations. This study, therefore, investigated whether genetic variation in key pharmacogenes influences the risk of treatment-related side effects in a South African breast cancer cohort. : A total of 166 women of Mixed and African Ancestry treated with 20 mg/day tamoxifen at Groote Schuur Hospital, South Africa, were included in the study. Genetic variation across 28 variants in nine pharmacogenes, including , , , , , and , was assessed using various genotyping methods. Associations between genetic and non-genetic factors and tamoxifen side effects were evaluated with logistic regression. : Over 70% of participants reported at least one treatment-related side effect. Overall side-effect burden was associated with copy number variation ( = 0.030) and rs3736599 ( = 0.042). Musculoskeletal complaints were the most common (40%) and were associated with rs7439366 ( = 0.040) and rs2242480 ( = 0.051). Gynecological symptoms affected more than 20% of participants and were linked to ( = 0.050), rs3736599 ( = 0.016), and rs4148269 ( = 0.039). Hot flashes were frequent, affecting 33% of patients, but showed no clear pharmacogenetic associations. : This study demonstrates that pharmacogenetic variation is associated with interindividual differences in treatment-related side effects, underscoring the need to expand research in African populations to better inform precision endocrine therapy. - Source: PubMed
Publication date: 2026/02/24
Kruger BiancaChimusa EmileAbera AronSingh JesmikaShamley DelvaDandara Collet - Alopecia is a prevalent condition that affects both sexes, characterised by miniaturisation of hair follicles and changes in the dynamics of the hair cycle, such as androgenetic alopecia associated with various systemic factors, including the COVID-19 pandemic. Minoxidil (base), initially developed as an oral antihypertensive, is currently used in the treatment of alopecia, acting as a prodrug that requires hepatic sulphation to generate its active metabolite, minoxidil sulphate. Topical formulations use minoxidil sulphate, the active pharmaceutical ingredient, directly on the hair follicles. Pharmacogenomic studies highlight the critical role of SULT1A1 enzyme variability in modulating treatment response, supporting personalised therapeutic strategies. Despite challenges related to low water solubility, high permeability, and narrow therapeutic index, emerging pharmaceutical technologies, including minitablets, orodispersible forms, sublingual preparations, and modified release systems, offer the potential to optimise absorption, increase dosing accuracy, and reduce adverse effects. This review consolidates current knowledge on the chemistry, pharmacology, pharmacogenomics, and technological aspects of minoxidil (base) for systemic use, emphasising translational developments that may redefine its clinical applications and contribute to safer and more standardised therapies. The integration of medicinal chemistry, pharmaceutical technology, clinical pharmacology, and regulatory guidance is expected to promote oral minoxidil as a reliable, effective, and patient-centred therapeutic option for alopecia. - Source: PubMed
Publication date: 2026/03/24
de Oliveira Gustavo TerraIkegaki Ana Beatriz Kimie Baioccode Souza Isadora Luziana IzidoroAgostini Sandra Barbosa NederMarques Maria Betânia de Freitasde Araújo Magali Benjamim - Although a range of glomerular diseases profoundly affect glomerulus-associated cells, a comprehensive understanding of their molecular alterations is still lacking. Here, we performed in-depth analysis of glomerular data from mouse models of primary and secondary glomerulopathies and constructed a multi-disease cellular landscape of glomerular cells. We identified a putative subset of proliferative glomerular endothelial cells(gECs) that highly expresses genetic susceptibility genes associated with multiple glomerular diseases. Podocytes exhibited shared injury-associated cell types across different disease models. A podocyte subset highly expressing , , , , , and was predominantly derived from ob/ob mice, whereas another podocyte subset with high expression of , , , , and was mainly observed in adriamycin-induced mice. Mesangial cells shared common injury-related alterations across diseases (high expression of , , , and ), while ob/ob mice exhibited a distinct mesangial cell subset (high expression of and ). In contrast, the gECs displayed similar molecular changes across different diseases without giving rise to disease-specific subtypes. Intercellular ligand-receptor analysis underpins the recruitment of immune cells by injured mesangial cells and podocytes via specific engagement of pairs such as CXCL and MIF, respectively. Our study systematically elucidates the molecular alterations of glomerulus-associated cells across various diseases, providing a foundation and strategic insights for future targeted therapies tailored to specific glomerular disease contexts. - Source: PubMed
Publication date: 2026/02/24
Huang YanLi ShuoLi ShuyingDuan ShuzhongHuang LanWang JingMa LiangyanLiu CeChen Qilin