SULT1A1 antibody Host Rabbit
- Known as:
- SULT1A1 (anti-) Host Rabbit
- Catalog number:
- 'H00006817-D01
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SULT1A1 antibody Host Rabbit
Related genes to: SULT1A1 antibody Host Rabbit
- 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 antibody Host Rabbit
Related articles to: SULT1A1 antibody Host Rabbit
- Increasing evidence supports associations between cognitive function and autoimmune disorders, yet the underlying genetic mechanisms remain unclear. Using large-scale genome-wide association statistics for seven cognitive traits and fifteen autoimmune disorders, together with two independent cohorts comprising 522 healthy individuals and 80 patients with schizophrenia, we performed multi-level pleiotropic analyses. Genetic correlation analyses identified nine significant cognition-immune linkage pairs, whereas Mendelian randomization (MR) analyses suggested that these associations were largely driven by shared genetic architecture rather than causality. Using PLACO, colocalization analysis, and MAGMA analyses, we identified 46 pleiotropic loci and 169 pleiotropic genes across the linkage pairs. Polygenic risk scores derived from pleiotropic variants were associated with cognition in healthy adults and showed nominal associations in schizophrenia. Enrichment analyses linked these genes to cognition-immune-related tissues, pathways, and biological processes, while multi-trait colocalization highlighted CD33 as a potential key mediator. Finally, summary-based MR analyses of both pleiotropic genes and anti-inflammatory drug target genes highlighted AMT, CRAT, ERAP2, ERBB3, GNL3, IRF3, MST1R, RPS26, SH2B1, SULT1A1, SULT1A2, TMEM258, CYP2D6 and MAPK3 as promising therapeutic targets for both cognitive function and autoimmune disorders. This study delineates the shared genetic architecture underlying the cognition-immune nexus and identifies novel candidate targets, highlighting the value of integrative genetic approaches for advancing diagnosis and treatment. - Source: PubMed
Publication date: 2026/07/01
Yu TongZhao GuoruiZhang YuyananSun YaoyaoLu ZheYuan RuiZhu YunqingKang ZheweiFeng XiaoyangSun JunyuanGuo JingYang YangYue Weihua - Heart failure (HF) is a heterogeneous syndrome with diverse etiologies, yet the metabolic determinants specific to its subtype remain unclear. We performed an integrative multi-omics analysis combining metabolomics, genetics, and single-cell transcriptomics to characterize metabolic signatures of distinct HF subtypes. By applying Mendelian randomization of 1,091 circulating metabolites, we identified distinct metabolic patterns: lipid metabolites, particularly sphingolipids, were associated with increased HF risk, while tricarboxylic acid (TCA) cycle intermediates exhibited potential protective effects. Subtype-specific differences included lipid remodeling in coronary heart disease (CHD)-related HF, TCA metabolism in hypertension (HTN)-related HF, and amino acid pathways in overweight-related HF. Integrative analyses highlighted candidate regulators such as UPP1, NEU3, CBS, SHMT1, PLD2, OGDHL, and SULT1A1/2. Single-cell data revealed cardiomyocyte-enriched expression of OGDHL, which was consistently downregulated in experimental HF models. These findings provide insight into metabolic heterogeneity in HF and identify OGDHL as a potential regulator of cardiac metabolic remodeling. - Source: PubMed
Publication date: 2026/06/30
Xue YuzhouLiu LinXu MingJin Ling - : Glucosinolates, secondary metabolites present in Brassicales, and their breakdown products have demonstrated various biological effects, including anti-carcinogenic activities in some animal models. The active compounds include indole-3-carbinol (I3C) and -methoxyindole-3-carbinol (NI3C). Building on these findings, several synthetic -substituted I3Cs strongly inhibited the growth of human cancer cell lines. This effect was mediated by reactive intermediates formed by sulphotransferase (SULT) 1A1. : We present genotoxicity findings on I3C and N-substituted derivatives, with special consideration given to SULTs. : We review genotoxicity findings with I3C, NI3C and their parental glucosinolates. Then, we present some findings hitherto unpublished. : Neoglucobrassicin and its breakdown product NI3C demonstrated high genotoxic activity in vitro and formed high levels of DNA adducts in animal studies. These effects were strongly enhanced in the presence of SULT1A1. By contrast, glucobrassicin and I3C were weakly mutagenic. New observations include: enhanced activation of NI3C to a mutagen by human SULT1C4 compared to SULT1A1; SULT1A1-dependent genotoxicity of I3C (induction of sister chromatid exchange, SCE); cellular co-localisation of SULT1A1 and DNA adducts formed in the kidneys of NI3C-treated mice. : I3C and NI3C are genotoxic in the presence of an appropriate SULT, but with large quantitative and qualitative differences (I3C required higher concentrations and induced only SCE, virtually no gene mutations). No information is available regarding the genotoxicity of other -substituted I3C derivatives being developed as antineoplastic drugs. We suspect that they may greatly vary in this activity, which in turn might impact clinical effectiveness as well as adverse side-effects. - Source: PubMed
Publication date: 2026/06/05
Glatt HansruediSchumacher Fabian - Metabolic syndrome (MetS) is a cluster of risk factors increasing the likelihood of cardiovascular and metabolic diseases. This study investigated the relative mRNA expression of key hepatic and intestinal phase II drug-metabolising enzymes, specifically UDP-glycosyltransferases (UGTs) and sulfotransferases (SULTs), in four non-obese rat models of MetS characterised by different dominant traits: the hereditary hypertriglyceridaemic (HHTg) rat, spontaneously hypertensive rat (SHR), SHR-expressing transgenic human C-reactive protein (SHR-CRP) rat, and bilaterally ovariectomised female Wistar (W-OVX) rat, compared to Wistar controls. Gene expression was quantified by RT-PCR with data normalised using the ΔΔCt method. Measurements showed significant model-specific differences, especially in the liver. HHTg rats exhibited significant hepatic suppression of (-90%) and undetectable transcripts, alongside compensatory upregulation of (196%) and (277%). The SHR model showed significant hepatic upregulation of (330%), (266%), and (328%). Chronic inflammation in SHR-CRP rats caused a significant decrease in hepatic , whereas a significant induction occurred in the intestine. Oestrogen deprivation (W-OVX) led to significant downregulation of hepatic and . These findings highlight that the alterations in phase II metabolism strongly depend on the pathophysiological context, potentially affecting drug disposition in preclinical models. - Source: PubMed
Publication date: 2026/05/27
Soukop JanPoruba MartinRácová ZuzanaZapletalová IvetaMalínská HanaHüttl MartinaMarková IrenaVečeřa Rostislav - 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