DHEA RIA
- Known as:
- DHEA RIA
- Catalog number:
- kipb1138
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Diasource
- Gene target:
- DHEA RIA
Related genes to: DHEA RIA
- 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 RIA
(Arg8)-Vasopressin - Diluted Antiserum for RIA(Arg8)-Vasopressin - Diluted Antiserum for RIA,(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - RIA Kit(Arg8)-Vasopressin - RIA Kit, Host Rabbit, CE-marked(Arg8)-Vasopressin - RIA Kit, Host RabbitCE-marked(Arg8)-Vasopressin - RIA Kit, Host: Rabbit, CE-marked(Arg8)-Vasopressin - RIA Kit, Host: Rabbit, CE-marked(Arg8)_Vasopressin _ Diluted Antiserum for RIA, Host Rabbit(Arg8)_Vasopressin _ Diluted Antiserum for RIA, Host Guinea Pig Related articles to: DHEA RIA
- Given the existing uncertainties regarding the link between Di(2-ethylhexyl) phthalate (DEHP) exposure and gastric cancer (GC) progression, this study aimed to clarify their association, identify the toxic targets of DEHP, and elucidate the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/07/16
Li ShenghaoPeng QingHao LiyuanMao JingyuHuo Bingjie - Disruption of bile acid (BA) homeostasis and circadian rhythm are interconnected in chronic liver diseases, yet how circadian dysfunction exacerbates cholestasis remains unclear. This study demonstrates that hepatocyte-specific knockout of the core clock gene Bmal1 in female mice markedly aggravates liver injury, inflammation, and fibrosis in an α-naphthylisothiocyanate (ANIT)-induced intrahepatic cholestasis model. The pathological exacerbation is attributed to a profound loss of circadian oscillation and reduced expression of the detoxification enzyme sulfotransferase family 2A member 1 (SULT2A1), resulting in deficient sulfation and hepatic accumulation of cytotoxic bile acids. This hypersusceptibility was further validated in primary hepatocytes under BA overload. Notably, specific in vivo restoration of hepatic SULT2A1 significantly reversed these pathological progressions. Mechanistically, BMAL1 transcriptionally activates Sult2a1 by directly binding to the E-box element within its promoter region. Taken together, our work elucidates the BMAL1-SULT2A1 axis as an essential circadian defense mechanism that maintains hepatic bile acid detoxification homeostasis in female mice, providing a novel theoretical basis for chronotherapeutic strategies in cholestatic liver diseases. - Source: PubMed
Publication date: 2026/07/15
Xiao YifeiHe JiatianZheng YiZhang XinyuLi JintaoJin MengChen MinWu YushanLiu XiaowenXu HaimanLin LuominWu BaojianGuo LianxiaDong Dong - 24S-hydroxycholesterol (24SOH-Chol) is a bioactive cholesterol metabolite formed in the brain. This endogenous activator of the cholesterol sensor, liver X receptor (LXR) is abundantly found as a sulfate-glucuronide diconjugate in the human plasma. The present study characterizes the human sulfonating (SULT) and glucuronidating (UGT) enzymes; and evaluates how these enzymes impact its ability to bind to and activate LXR. In vitro enzymatic assays identified the human SULT2A1 and UGT1A4 as the major isoforms for hepatic 24SOH-Chol sulfonation and glucuronidation, respectively. Additional assays demonstrated that 24SOH-Chol-3Sulfate,24Glucuronide formation requires the successive involvement of UGT1A4 and SULT2A1. TR-FRET and transient transfection experiments revealed that glucuronidation, but not sulfonation, inactivates 24SOH-Chol. Exposure of human liver cells and humanized UGT1 mice to LXR ligands identified UGT1A4, but not SULT2A1, as a positively regulated LXR target gene, while chromatin immunoprecipitation assays, luciferase reporter and siRNA knock down assays demonstrated the ability of LXR to bind to and activate the human UGT1A4 gene promoter. The present study establishes the complementary roles played by SULT2A1 and UGT1A4 in 24SOH-Chol conjugation. We also identify glucuronidation as a mechanism allowing this cholesterol derivative to self-stimulate its own inactivation. - Source: PubMed
Publication date: 2026/07/13
Brousseau ValérieRettenmeier EvaVerreault MélanieTrottier JocelynChen ShujuanTukey Robert HBarbier Olivier - Liver fibrosis is a reversible phase of arsenic-induced chronic liver injury, with bile acid metabolic alterations closely associated with this pathological process. SIRT1 is a key metabolic regulator and promising therapeutic candidate, while its role in bile acid metabolism during arsenic-induced liver fibrosis remains poorly defined. This study established time-dependent rat models of arsenic-induced liver fibrosis with resveratrol intervention to investigate the potential association between SIRT1, bile acid metabolic disturbance, and liver fibrosis, as well as resveratrol's hepatoprotective effects. Arsenic exposure induces progressive accumulation of hydrophobic bile acids in the liver, inflammation, hepatic stellate cell activation, and fibrosis, accompanied by suppressed expression of bile acid phase II detoxification genes (, , ) and the bile acid efflux transporter gene (BSEP). Arsenic exposure reduces SIRT1 expression and increases C/EBPα acetylation, which may relate to impaired transcription of the aforementioned bile acid metabolic genes. Resveratrol may restore SIRT1 expression, normalize C/EBPα acetylation and bile acid homeostasis, and reduce hepatic arsenic accumulation, thereby alleviating liver fibrosis. Collectively, the SIRT1/C/EBPα axis and bile acid metabolism may be linked to the progression of arsenic-induced liver fibrosis. Resveratrol may exert protective effects via multiple mechanisms, including regulating these molecular targets and reducing hepatic arsenic accumulation. - Source: PubMed
Publication date: 2026/06/05
Wang QiChen HualinRan QimingHu FangFu QiwenMa Lu - Childhood obesity is rising globally. Yet, few studies have examined the microbiome and proteome in early childhood in relation to this outcome, and most are cross-sectional by design. Early-life factors in the ABIS birth cohort ( = 16,683) were associated with obesity up to age 26 (mean follow-up 25.3 years, range 23.7-26.5 years): psychosocial stressors, smoking, infections, and diet in the first year. We assessed biomarkers, including cord blood metabolome ( = 290) and proteome ( = 358), by liquid chromatography, mass spectrometry, and Olink. Gut microbial composition at age one ( = 1,743) was assessed using stool samples and 16S rRNA sequencing. In this prospective longitudinal cohort study, significant differences were found in infants with future obesity, including elevated angiopoietin-like 4 (ANGPTL4), follistatin, and hepatocyte growth factor (independently of maternal weight) and reduced isocaproic acid, tryptophan, and oleic acid, with prenatal mediation. , asaccharolytic bacteria ( and ), and equol-producers ( and ) were depleted. Machine learning models selecting 40 most predictive features showed long-term prediction from birth proteomics and bacterial taxa at age one (area under the curve [AUC] = 0.83 ± .05, = 1,877) and additional metrics, for example, parental and child body mass index in the first 8 years (AUC = 0.89 ± .02, = 1,877), suggesting durable biological encoding. Proteomic markers across folds included fibroblast growth factor 19, ANGPTL4, sulfotransferase family 2A member 1, and interleukin 20. These findings suggest clinically relevant biomarkers indicating early-life regulation of bile acid metabolism, lipid storage vs. oxidation, and immune-metabolic signaling and pathways to prospectively prevent childhood- and adult-onset obesity across a 26-year predictive gap. - Source: PubMed
Publication date: 2026/05/28
Ahrens Angelica PDias RaquelHyötyläinen TuuliaWhite Pär AndersonOrešič MatejTriplett Eric WLudvigsson Johnny