DHEA_S
- Known as:
- DHEA_S
- Catalog number:
- C18-315
- Product Quantity:
- 96 Tests
- Category:
- -
- Supplier:
- Immunospec
- Gene target:
- DHEA_S
Related products to: DHEA_S
5-Androsten-3beta-OL-7, 17-Dione (DHEA) Antibody7a_Hydroxy DHEA 7a_Hydroxy DHEA7_Keto dehydroepi androsterone Keto DHEAAcP_ DHEAAnti- Dehydroepiandrosterone (DHEA) Sulfate-3 AntibodyAnti- Dehydroepiandrosterone (DHEA) Sulfate-7 AntibodyAntibody to Dehydroepiandrosterone (DHEA) Organism: Homo sapiens (Human) Type: Polyclonal Source: RabbitAntibody to Dehydroepiandrosterone (DHEA) Organism: Homo sapiens (Human) Type: Polyclonal Source: RabbitAntimicrobial Drugs: Natural Steroids: DEHYDROEPIANDROSTERONE SULPHATE (DHEA-S), Host animal: Sheep, Format: Purified monoclonal antibodyAntimicrobial Drugs: Natural Steroids: DEHYDROEPIANDROSTERONE SULPHATE (DHEA-S), Host animal: Sheep, Format: Purified monoclonal antibodyBile salt sulfotransferase,Dehydroepiandrosterone sulfotransferase,DHEA-ST,Homo sapiens,HST,HST,Human,Hydroxysteroid Sulfotransferase,ST2,ST2A1,ST2A3,STD,Sulfotransferase 2A1,SULT2A1Biotin-linked Antibody to Dehydroepiandrosterone (DHEA); Reactivity: Homo sapiens (Human) Clonality: Polyclonal Source: RabbitBovine Dehydroepiandrosterone ELISA , DHEABovine Dehydroepiandrosterone ELISA , DHEABovine Dehydroepiandrosterone(DHEA)ELISA Kit Related articles to: DHEA_S
- Hepatic lipid accumulation (steatosis) is an early indicator of non-alcoholic fatty liver disease (NAFLD), preceding fibrosis and cirrhosis. Understanding its effects on drug-me-tabolizing enzymes (DMEs) and transporters is crucial for assessing potential alterations in drug dis-position among NAFLD patients. This study aimed to replicate steatosis in an in vitro HepaRG cell model and analyze its impact on DMEs and transporters. - Source: PubMed
Publication date: 2025/09/09
Saravanakumar AnithaTierney Cassandra AHe WenJamwal RohitashBarlock BenjaminBush XinJohnson Jillian GRodrigues David AAkhlaghi Fatemeh - Aortic stenosis (AS) involves aortic obstruction, pressure overload, reduced cardiac output, and impaired organ arterial hemodynamics. Many patients remain at risk of rehospitalization or death after transcatheter aortic valve replacement (TAVR) due to unclear mechanisms. Our previous studies linked bile acids (BAs) metabolism to heart-other organ crosstalk, but the BAs-hemodynamics interplay in AS remains unclear. - Source: PubMed
Publication date: 2025/09/09
Zhu MinHua KunWang HuiqingGuan ZhiyuanTong ZexinGao JuanShi QuanyouWang HuYan ShenLiu YuhuaShi QingqingXu TanWang JiaxingChang TianqiXue YuzhouZhao YaoboFu YiwenZheng HuipingFeng XinhengShang ShaomeiWang Xiu-JieWang Shi-QiangZhang ZheLan FengJiang ChangtaoYang XiubinZheng LeminXu Ming - Sulfotransferase (SULT) enzymes contribute significantly to drug metabolism in pediatric patients. The purpose of this study was to develop a PBPK model for acetaminophen (APAP) in pediatric populations that accounts for the ontogeny of SULT isozymes that play a critical role in APAP metabolism. PBPK modeling and simulation were performed using the Simcyp Simulator. The model incorporated the developmental ontogeny of three key hepatic SULT enzymes: SULT1A1, SULT1A3, and SULT2A1 using "best-fit" ontogeny equations for each isozyme as determined by nonlinear regression analysis of enzyme abundance versus age. PBPK model-simulated pharmacokinetic profiles for APAP captured observed clinical data for systemic exposure (Cmax, AUC) in neonates, infants, and children. SULTS accounted for ~60% APAP metabolism in neonates, with decreased contributions to infants and children. Model sensitivity analysis highlighted the potential for APAP metabolic DDIs, primarily through SULT1A1. The study demonstrates that the impact of SULT enzymes on drug metabolism is significant in neonates, which is an important clinical consideration for APAP. A PBPK model that incorporates SULT ontogeny has the potential to help inform dosing decisions in this special patient population. - Source: PubMed
Publication date: 2025/07/13
Sharma SoniaTaft David R - Frailty is a multifactorial condition highly prevalent in patients with chronic kidney disease (CKD), increasing with disease progression. Identifying genetic determinants associated with frailty may aid in risk stratification. We aimed to identify whether single nucleotide polymorphisms (SNPs), individually or combined into a genetic risk score (GRS), are associated with the frailty phenotype and adverse clinical outcomes in CKD patients. - Source: PubMed
Publication date: 2025/07/21
Rodrigues Hellen Christina NevesCoelho Alexandre Siqueira GuedesFreitas Ana Tereza Vaz de SouzaPeixoto Maria do Rosário GondimHorst Maria AderuzaCosta Nara Aline - Cholestasis, a major driver of liver disease progression, is characterized by toxic bile acid accumulation due to impaired bile flow, potentially leading to hepatic fibrosis, cirrhosis, and hepatocellular carcinoma. To date, the pathogenesis of cholestasis has remained incompletely understood. In the present study, we investigated the role of farnesoid X receptor (FXR) in modulating the NLR family CARD domain-containing protein 4 (NLRC4) inflammasome activity using in vitro (AML-12 hepatocytes) and in vivo (C57BL/6 mice) models of lithocholic acid (LCA)-induced cholestasis. LCA suppressed FXR expression, downregulated bile acid transporters (Bsep, Mrp2, Ntcp), and elevated serum biomarkers of liver injury. Through restored hepatic function by FXR lentiviral vectors, FXR overexpression reduced bile acid accumulation and mitigated inflammation and oxidative stress. In addition, FXR overexpression suppressed bile acid synthesis enzymes (Cyp7a1, Cyp8b1) by upregulating Shp and Fgf15, while enhancing detoxification through Ugt1a1 and Sult2a1. Interestingly, molecular docking analysis and Co-IP experiments demonstrated a direct interaction between FXR and NLRC4. Furthermore, FXR overexpression significantly inhibited NLRC4 inflammasome activation and decreased the expression of NLRC4, caspase-1, IL-1β, and IL-18, thereby attenuating inflammation and oxidative stress. Conversely, FXR knockdown reversed these effects. In addition, to delineate the contribution of NLRC4 inflammasome activation to IL-18 and IL-1β elevation, NLRC4-targeting siRNA-mediated knockdown and NLRC4-encoding plasmid-driven overexpression strategies were systematically employed. Furthermore, DCFH-DA staining was adopted to visualize reactive oxygen species (ROS). In conclusion, for the first time, we found that FXR overexpression alleviates LCA-induced cholestasis by regulating bile acid metabolism and inhibiting NLRC4 inflammasome activation, providing a novel therapeutic strategy for drug development targeting the FXR-NLRC4 axis. - Source: PubMed
Publication date: 2025/06/22
Wang WenyuLi LinLi XiaChen JiaqiWang RuiYang QiQu YifanWang ChangyuanFu TingMeng Qiang