DHEA_S
- Known as:
- DHEA_S
- Catalog number:
- BQ 079S
- Product Quantity:
- 96/kit
- Category:
- -
- Supplier:
- Bioquant
- 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
- 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 - Immune checkpoint blockade (ICB) unleashes antitumor immunity but frequently provokes enduring endocrine toxicities. We hypothesize that ICB accelerates adrenal aging by establishing chronic low-level inflammation within the adrenal cortex, with targeting vulnerability of the zona reticularis. Integrating a recently published human multiorgan aging proteome atlas and primate adrenal aging study with survivorship data after ICB therapy, we propose a testable signaling cascade: ICB-amplified interferon gamma (IFNγ)/ tumor necrosis factor (TNF)/ interleukin-1 signaling activates nuclear factor kappa B (NF-κB)/signal transducer and activator of transcription 1 (STAT1), suppressing sterol regulatory element-binding protein 2 (SREBP2)-low-density lipoprotein receptor (LDLR)-mediated cholesterol uptake; concurrent mitochondrial/endoplasmic reticulum stress drives proteome-transcriptome decoupling, loss of cytochrome b5 type A (CYB5A), and impaired cytochrome P450 family 17 subfamily A member 1 (CYP17A1) 17,20-lyase activity; inflammatory transcriptional repression of sulfotransferase family 2A member 1 (SULT2A1) with proteostasis decay reduces dehydroepiandrosterone (DHEA) sulfation. The net result is a persistent fall in DHEA/DHEA sulfate (DHEAS) with comparatively preserved cortisol-mirroring natural adrenal aging. We advocate prospective measurement of DHEAS, DHEA, adrenocorticotropic hormone (ACTH), and cortisol at baseline, during therapy, end of therapy, and 6-24 months post-therapy; if early DHEAS decline is confirmed, targeted interventions including DHEA replacement or glucocorticoid receptor antagonism warrant evaluation. This framework reframes certain endocrine immune-related adverse events as "accelerated organ aging," with implications for risk stratification, toxicity prevention, and survivorship care. - Source: PubMed
Publication date: 2026/04/27
Ding GuanxiongXu YangyangGuo TingFeng Chenchen - : Tamoxifen is widely used in the treatment of hormone receptor-positive breast cancer and has been shown to successfully reduce recurrence and mortality rates. Nonetheless, variability in patient response to tamoxifen treatment is observed with up to 40% of patients experiencing recurrence. Genetic polymorphisms in pharmacogenes encoding enzymes involved in tamoxifen metabolism have been linked to some of this observed interindividual variability. The pharmacogenetics of tamoxifen in populations of African descent remain understudied, creating difficulties in pinpointing the primary factors behind the observed variable response. To address this gap, this study aimed to investigate the role of genetic variation in tamoxifen treatment outcomes in a South African cohort. : Participants included 166 Mixed and African Ancestry breast cancer patients who had received tamoxifen treatment. Genetic characterization was performed for 53 single nucleotide polymorphisms (SNPs) and two copy number variations across eight drug-metabolizing enzymes, including cytochrome P450s (, , , ), UDP-glucuronosyltransferases (), and sulfotransferases (, , ). The association between genotypes and disease-free survival (DFS) was evaluated using Cox proportional hazards regression models. : The or * genotype showed a nominal association with improved DFS ( = 0.049), with a similar trend observed for rs11888492. In contrast, rs3775779 heterozygosity showed a nominal association with reduced DFS ( = 0.044). SNPs (rs4149393, rs4149394, rs1042157) demonstrated trends toward reduced DFS. : These exploratory findings highlight the need for more inclusive pharmacogenomic research and point to potential biomarkers for optimizing tamoxifen therapy in African populations. - Source: PubMed
Publication date: 2026/03/31
Kruger BiancaChimusa Emile RAbera Aron BSingh JesmikaShamley DelvaDandara Collet - 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