SULT1A1
- Known as:
- SULT1A1
- Catalog number:
- ARP49134_P050
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SULT1A1
Related genes to: SULT1A1
- 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
anti-SULT1A1anti-SULT1A1anti-SULT1A1anti-SULT1A1anti-SULT1A1 (1F8)anti-SULT1A1 (1F8)anti-SULT1A1 type: Primary antibodies host: Mouseanti-SULT1A1 type: Primary antibodies host: RabbitAryl sulfotransferase 1,HAST1_HAST2,Homo sapiens,Human,OK_SW-cl.88,Phenol sulfotransferase 1,Phenol-sulfating phenol sulfotransferase 1,P-PST 1,ST1A1,ST1A3,STP,STP1,Sulfotransferase 1A1,SULT1A1,ThermoAryl sulfotransferase,Aryl sulfotransferase IV,ASTIV,Minoxidil sulfotransferase,Mx-ST,Phenol sulfotransferase,PST-1,Rat,Rattus norvegicus,ST1A1,St1a1,Sulfokinase,Sulfotransferase 1A1,Sult1a1,Tyrosine-Aryl sulfotransferase,Bos taurus,Bovine,Phenol sulfotransferase,Phenol-sulfating phenol sulfotransferase,P-PST,ST1A1,STP,Sulfotransferase 1A1,SULT1A1Aryl sulfotransferase,Canis familiaris,Canis lupus familiaris,Dog,Phenol sulfotransferase,Phenol-sulfating phenol sulfotransferase,P-PST,ST1A1,Sulfotransferase 1A1,SULT1A1Aryl sulfotransferase,Mouse,mSTp1,Mus musculus,Phenol sulfotransferase,Phenol_aryl sulfotransferase,ST1A1,St1a1,ST1A4,Stp,Stp1,Sulfokinase,Sulfotransferase 1A1,Sult1a1Bovine Sulfotransferase 1A1(SULT1A1) ELISA kitBovine Sulfotransferase 1A1(SULT1A1) ELISA kit SpeciesBovine Related articles to: SULT1A1
- To investigate the causal relevance of melatonin metabolism, which provides the biological basis for circulating melatonin levels, to specific depression symptom subtypes, we performed a targeted systematic review of melatonin metabolism pathways in the human brain and liver. Using two-sample Mendelian randomization (MR), we assessed the causal effects of metabolism pathways and/or individual genes on major depressive disorder (MDD) and nine symptom subtypes derived from Patient Health Questionnaire-9 (PHQ-9). Instrumental variables (IVs) were expression quantitative trait loci (eQTL) for eight individual genes, one synthesis route, and three degradation routes. Results were assessed using Bayesian colocalization and phenome-wide association analyses. At the pathway-level, the genetically proxied synthesis-route signal was associated with PHQ-9 Assessment 5 (PHQ9A5, OR: 0.89, 95% CI: 0.85-0.93), but sensitivity analyses suggested this association was primarily driven by TPH1 and may reflect serotonin-related biology. In contrast, higher brain melatonin degradation raised the risk of both PHQ9A1 (OR: 1.03, 95% CI: 1.02-1.04) and PHQ9A7 (OR: 1.03, 95% CI: 1.02-1.03). Within degradation, up-regulation of the kynurenine sub-pathway increased the odds of PHQ9A3 (OR: 1.05, 95% CI: 1.02-1.07), PHQ9A4 (OR = 1.04, 95% CI: 1.02-1.06) and PHQ9A7 (OR: 1.05, 95% CI: 1.02-1.07). Gene-level analyses were largely concordant, except for SULT1A1, whose higher expression was genetically protective for PHQ9A3 but risk-increased for PHQ9A1 and PHQ9A4. Overall, these results demonstrate that melatonin metabolism exerts symptom-specific and pathway-specific causal effects on depression. A stratified view of melatonin's role may help optimize the application of exogenous melatonin supplementation. - Source: PubMed
Publication date: 2026/07/30
Wang YuanbiWen WenChen HanshengJin YangyangCao JiechengChen WenzhongCai LeiHe Lin - During development, entry of any substances from the circulation into the brain is tightly regulated by a series of blood-brain interfaces. Notably, the choroid plexuses, which form the blood-cerebrospinal fluid barrier, serve as a key interface for molecular exchange in early life. Control mechanisms within the choroid plexuses include efflux transporters and conjugating enzymes, such as glutathione S-transferases and UDP-glucuronosyltransferases, which have been shown to play key roles in safeguarding the developing brain. Sulphotransferases are another family of conjugating enzymes reported to be highly expressed in the choroid plexus in humans and rats during development. However, their activity and functional significance in the central nervous system remain poorly understood. In the present study, sulphotransferase activity was measured in the lateral and fourth ventricle choroid plexus from rats at embryonic Day 19 and postnatal Day (P)1, 3, 8 and 30. Activity was correlated with expression of isoenzymes by RT-qPCR. Inhibition studies were performed by co-incubating a prototypical sulphotransferase substrate with a potential substrate or inhibitor. Finally, assays in freshly isolated live tissue were conducted to assess sulphoconjugation under more physiologically relevant conditions. Results showed that both sulphotransferase activity and expression of Sult1a1 in the choroid plexus were markedly increased at P1 to P3. This distinct temporal pattern suggests age- and tissue-specific roles of choroidal sulphotransferase activity during the early postnatal period. Interactions with xenobiotics and neuroendocrine factors further suggest that these enzymes may contribute to multiple processes during this critical window, including protection against potentially harmful substances and regulation of neurotransmitters. Furthermore, the observed modulation of choroidal sulphotransferase activity by various exogenous substances suggests that developmental exposure could disrupt sulphotransferase-mediated biological processes, with potential consequences for normal neurodevelopment. - Source: PubMed
Qiu FionaStrazielle NathalieDenuziere AnneGhersi-Egea Jean-François - Circadian disruption is increasingly recognized as a contributing factor in tumorigenesis and tumor evolution; however, the role of circadian genes in osteosarcoma cell fate determination and therapeutic response remains to be fully elucidated. - Source: PubMed
Publication date: 2026/07/07
Xie JunQian ChaoGuo JinkuWang WeiChen ChenPeng RenjieXu Ankai - 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