Ask about this productRelated genes to: DHEA 17-HRP
- Gene:
- SULT2A1 NIH gene
- Name:
- sulfotransferase family 2A member 1
- Previous symbol:
- STD
- Synonyms:
- DHEA-ST
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1994-03-03
- Date modifiied:
- 2016-10-05
Related products to: DHEA 17-HRP
(ß)_hCG, HRP Conjugate- Agrisera HRP-Conjugate/Protein Stabilizer (100ml)- Agrisera HRP-Conjugate/Protein Stabilizer (10ml)- Agrisera HRP-Conjugate/Protein Stabilizer (1L)1 β Polyclonal Antibody, HRP conjugated Isotype: IgG1-Aminohydantoin (AHD)-HRP Conjugate1-Aminohydantoin (AHD)-HRP Conjugate1-step Polymer HISTO-STAT Peroxidase (HRP) Multivalent AEC kit for IHC staining of Mouse, Rabbit & Rat primary antibodies, 900 plus slides (large s1-step Polymer HISTO-STAT Peroxidase (HRP) Multivalent AEC kit for IHC staining of Mouse, Rabbit & Rat primary antibodies, 350 plus slides (small size1-step Polymer HISTO-STAT Peroxidase (HRP) Multivalent DAB kit for IHC staining of Mouse, Rabbit & Rat primary antibodies, 350 plus slides (small size1-step Polymer HISTO-STAT Peroxidase (HRP) Multivalent DAB kit for IHC staining of Mouse, Rabbit & Rat primary antibodies, 900 plus slides (large size1-step Polymer HISTO-STAT; HRP anti Hamster (Secondary Reagent Component) for staining Hamster antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP (Secondary Reagent Component) for staining Mouse, Rabbit & Rat antibodies 350 plus slides1-step Polymer HISTO-STAT; HRP (Secondary Reagent Component) for staining Mouse, Rabbit & Rat antibodies, 900 plus slides1-step Polymer HISTO-STAT; HRP anti Chicken (Secondary Reagent Component) for staining Chicken antibodies, 250 plus slides Related articles to: DHEA 17-HRP
- Severe alcohol-related hepatitis (sAH) is associated with high short-term mortality. However, 30-40% of patients fail to respond to corticosteroids, the only proven pharmacological treatment. The pathophysiological mechanisms underlying sAH and the marked heterogeneity in treatment response remain incompletely understood. We aimed to define cellular changes associated with corticosteroid response in sAH and to identify baseline markers predictive of treatment outcome. - Source: PubMed
Publication date: 2026/04/20
Van Melkebeke LukasBoesch MarkusOstyn TessaHuang WenxinAkkaya Cansuvan Sligtenhorst MatthiasEl Abyad DaniaSafaeifard FatemeDumarey AlexanderWallays MarieBoeckx BramFeio-Azevedo RitaSmets LenaGustot ThierryTrepo EricMoreno ChristophePutignano AntonellaLasser LucColle IsabelleDeltenre PierreMarot AstridTopal BakiClaus EvelineBonne LawrenceMaleux GeertScheele ColindaHendrikx TimNevens FrederikKorf HannelieRoskams TaniaDenadai-Souza AlexandreLambrechts DietherGovaere OlivierVan der Merwe SchalkVerbeek Jef - Cholestatic liver diseases, such as primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and biliary atresia (BA), are characterized by bile accumulation and frequently progress to liver fibrosis, cirrhosis, and organ failure. - Source: PubMed
Publication date: 2026/04/09
Pan DiZheng TianChen CanpingQiu JieDeng ZhijuanJiang ZhaohuiChen YanXiao ChaodaXu YiniFu LingyunLinghu KegangChen JiyuFan FangfangZhang QingxiuTao LingHu XiaoxiaZhao LiShen Xiangchun - Our previous work revealed that the anti-diarrhea effects of alkaline mineral complex (AMC) water improve metabolism and protect the gut during weaning stress. However, whether AMC water can inhibit viral replication and treat viral diarrhea is unknown. The aim of this study was to explore the ability of AMC water to improve nutrient metabolism and protect against infection. In this study, porcine epidemic diarrhea virus (PEDV) or porcine deltacoronavirus (PDCoV) were used as RNA model viruses, and pseudorabies virus (PRV) or porcine circovirus (PCV) were used as DNA model viruses. Compared with those in the infected group, the virus content in the piglets fed AMC water was reduced, and the intestinal mucosal barrier was repaired. Transcriptome and metabolome results revealed that AMC water regulated lipid metabolism through GPAT2, DGKA, OAT3, FXR, LIPC and SULT2A1. Further studies showed that glycerol, cholesterol, and bilirubin levels increased after viral infection, and that AMC water inhibited cholesterol content and promoted bile acid synthesis. In a cellular model, AMC water reduced lipid droplet density by activating the glycerolipid and bile secretion pathways of the GPAT2/SULT2A1 axis. In addition, knockdown of DGKA and overexpression of SULT2A1 significantly affected the expression of the GPAT2/SULT2A1 axis, and the expression of viral proteins colocalized with lipid droplets was significantly decreased. Our findings suggest that AMC water promotes cholesterol metabolism by activating the GPAT2/SULT2A1 axis, inhibiting viral infection in piglets. This study provides theoretical support for the use of nutritional regulation to inhibit viral infection and provides a new method for antiviral therapy. - Source: PubMed
Publication date: 2026/03/11
Yao XinLi Nuo-WaLiu Ying-YingMalhi Kanwar KumarZhang Tian-TianZhao YangLi Hui-XinLi Jin-Long - Acetaminophen (APAP) overdose has become a leading cause of acute liver failure (ALF) in the United States and Europe. Alismatis rhizoma, the dried rhizome of Alisma orientale (Sam.) Juzep. or Alisma plantago-aquatica Lin, is a traditional medicinal herb. Our previous studies demonstrated that refined polysaccharides derived from Alismatis rhizoma exerted protective effects against APAP-induced liver injury. Nevertheless, the structures, biological activities, and structure-activity relationships of its glycans remained to be elucidated. In the present study, four novel glycans, designated ARP70-1, ARP70-2, ARP70-3, and ARP70-4, were isolated from Alismatis rhizoma. These polysaccharides were primarily composed of arabinose and galactose, with the predominant moieties identified as α-Araf-(1→, →5)-α-Araf-(1→, →3)-β-Galp-(1→, →6)-β-Galp-(1 → and →4,6)-β-Galp-(1→. In vitro experiments demonstrated that arabinogalactans mitigated APAP-induced injury in HepG2 cells by enhancing the levels of GSH, SOD, and CAT, while reducing MDA production. In vivo pharmacological evaluation of ARP70-1 using an APAP-induced acute liver injury mouse model showed that ARP70-1 enhanced hepatic antioxidant capacity, reduced inflammatory cytokine levels, and increased the abundance of beneficial intestinal bacteria, including Muribaculum, Prevotellaceae_UCG_001, Bacteroides, Parabacteroides, and Ruminococcus_torques_group. Additionally, ARP70-1 elevated intestinal levels of short-chain fatty acids (SCFAs) such as acetate, propionate, isobutyrate, 2-methylbutyrate, and isovalerate. Moreover, ARP70-1 promoted the hepatic expression of genes involved in bile acid metabolism and transport (CYP7A1, SLC10A1, ABCB11, ABCC3, BAAT, SULT2A1, and SULT2A8), and increased the levels of conjugated bile acids, including tauro-ursodeoxycholic acid (TUDCA), tauro-chenodeoxycholic acid (TCDCA), tauro-ω-muricholic acid (TωMCA), tauro-hyodeoxycholic acid (THDCA), and tauro-deoxycholic acid (TDCA). These effects collectively improved bile acid synthesis, transport, metabolism, and excretion, alleviated APAP-induced cholestasis, and conferred hepatoprotective effects. - Source: PubMed
Publication date: 2026/01/04
Lei PengZhang QingruiZhang XiaoxiaoJiang QibaoLi XiaogeJiang Miaomiao - Phenotypic age, an aging indicator derived from clinical biomarkers, is associated with morbidities and mortality. However, a liver-specific phenotypic aging indicator is still lacking, and its longitudinal associations with liver-related outcomes, as well as the underlying biological mechanisms, remain elusive. We developed a liver-specific phenotypic age using 11 selected clinical blood markers within the England-White cohort of the UK Biobank and validated this metric in both the Scotland-Wales cohort and Non-White-British cohort. We calculated phenotypic age acceleration (PhenoAgeAccel) and examined its association with long-term liver-related outcomes. We also explored the extent to which liver-specific PhenoAgeAccel mediated the impact of modifiable risk behaviors on liver-related outcomes. The metabolic and proteomic signatures of liver-specific PhenoAgeAccel were subsequently characterized. Liver-specific PhenoAgeAccel was significantly associated with a 1.23- to 2.97-fold increased risks of all-cause mortality and liver-related events. The impact of liver-specific PhenoAgeAccel on liver outcomes were more pronounced in males and in individuals with high genetic risk compared to their respective counterparts, and was stronger than that observed with systemic PhenoAgeAccel. Approximately 10-27% of the associations between risk behaviors and liver-related outcomes were mediated by liver-specific PhenoAgeAccel. Proteomic analysis identified 211 proteins associated with both liver-specific PhenoAgeAccel and liver-related outcomes, of which 22 (e.g., AGXT and SULT2A1) were liver-enriched and significantly mediated this relationship. Liver-specific PhenoAgeAccel is a strong predictor of liver-related outcomes, partially mediates the impact of modifiable behaviors, and is linked to liver-enriched proteins. This accessible tool may enhance risk stratification and support preventive strategies targeting liver health and aging. - Source: PubMed
Publication date: 2026/01/28
Wu TianhaoGuo ChengnanYuan HuangboDu MingyiZhang TiejunChen XingdongLiu Zhenqiu