Ask about this productRelated genes to: HSD3B2 antibody
- Gene:
- HSD3B2 NIH gene
- Name:
- hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 2
- Previous symbol:
- -
- Synonyms:
- SDR11E2
- Chromosome:
- 1p12
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-10
- Date modifiied:
- 2014-11-18
Related products to: HSD3B2 antibody
Related articles to: HSD3B2 antibody
- A six-gene panel involved in androgen production, uptake, and conversion (APUC-6: , , , , , ) may define distinct clinical outcomes in metastatic prostate cancer. This study evaluated the prognostic and predictive value of APUC-6 expression in metastatic castration-sensitive prostate cancer (mCSPC). - Source: PubMed
Publication date: 2026/08/21
Shi XiaoleiShetty Amol CWang JareySong YangSutera Philip ADeek Matthew PPatel Krishnan RMadan Ravi ATang ChadProudfoot JamesDavicioni ElaiHussain ArifNguyen PaulSweeney ChristopherBoytim EllaLacuna Kristine PRyan Charles JAntonarakis Emmanuel STran Phuoc THwang Justin - The human gut microbiome plays a critical role in immune regulation, yet the molecular links between microbiome composition and host gene expression remain incompletely understood. We analyzed associations between host gene expression and microbiome composition in a cohort of 315 healthy individuals, integrating microarray-based gene expression data from three intestinal sites (ileum, transverse colon, and rectum) and six immune cell types with microbiome sequencing data. Using a hierarchical feature aggregation strategy combining principal component analysis, clustering, and covariate correction, we discovered significant associations primarily related to immunity. While microbial profiles were similar across the three intestinal sites, the transverse colon yielded the most "microbiome-host gene expression" associations. Among the immune cell types, CD8+ cells showed the highest number of associations. The first principal component of microbiome composition, reflecting a gradient from commensals (e.g., and ) to proinflammatory taxa ([] and ), correlated with the expression of TNF-α-linked genes (, , , and ). Among individual genera, abundance was associated with gene expression in both intestinal and immune cells, including negative associations with MRPS21 (related to mitochondrial function) in the transverse colon and with CD8+ gene programs related to T cell differentiation. These findings align with emerging evidence implicating mitochondrial dysfunction in intestinal inflammation. Our results identify multi-level associations between the gut microbiome and host gene expression, suggesting potential mechanisms by which microbiota shape local and systemic immunity and vice versa. The implicated genes and taxa represent candidates for experimental validation to improve understanding of host-microbiome homeostasis and its disruption in disease.IMPORTANCEThe gut microbiome and immune system are engaged in a complex interplay throughout human life. While most associative studies focus on case-control comparisons-typically examining patients with conditions such as inflammatory bowel disease or metabolic diseases-less is known about the molecular links between the microbiome and immune system in healthy individuals. In this study of a large cohort of healthy individuals, we addressed this gap by applying multiscale modeling to tackle the high dimensionality of host-microbiome data. We identified multi-level associations between microbiome composition and host gene expression in both intestinal tissues and immune cells. These findings offer a valuable reference for understanding baseline host-microbiome communication and highlight molecular candidates-such as TNF-α-related genes and mitochondrial pathways-for future experimental validation. - Source: PubMed
Publication date: 2026/08/10
Shagam Lev IElizarova AnnaMomozawa YukihideDmitrieva JuliaMariman RobRahmouni SouadLouis EdouardGeorges MichelTyakht Alexander VKlimenko Natalia - This study aimed to characterize phase-specific dynamics of androstenedione and estradiol across IVF/ICSI treatment, identify predictors of reproductive outcomes, and examine the effects of follicle-stimulating hormone (FSH), IGF1, and estradiol on steroidogenesis in human granulosa-like tumor (KGN) cells. In women undergoing IVF/ICSI (10 successful and 19 unsuccessful), serum hormones were measured before recombinant FSH stimulation (Phase 1) and during the mid-follicular (Phase 2) and ovulatory (Phase 3) phases, with follicular fluid (FF) collected at Phase 3. Mechanistic experiments were conducted in KGN cells (n = 3) treated for 24 h. Successful pregnancy was associated with greater increases in androstenedione and estradiol from Phase 2 to Phase 3 and higher Phase 3 steroid-to-basal gonadotropin ratios. Elevated Phase 1 androstenedione and estradiol were negatively correlated with the number of retrieved oocytes, mature oocytes, and/or embryos. Phase 3 serum androstenedione (cutoff ≥ 2.382 ng/mL; AUC = 0.708, P = 0.038) and FF aromatase (cutoff ≤ 0.378 ng/mL; AUC = 0.727, P = 0.007) predicted clinical pregnancy. In KGN cells, IGF1 stimulated early steroidogenesis (HSD3B2 mRNA expression and progesterone levels), FSH enhanced both early and late pathways (HSD3B2 and CYP19A1 mRNA expression together with progesterone, androstenedione, and aromatase levels), and supraphysiological estradiol suppressed downstream steroidogenesis (CYP19A1 mRNA expression and aromatase and progesterone levels). In conclusion, a favorable pattern with low early-follicular and high late-follicular androstenedione and estradiol was associated with IVF/ICSI success, whereas high early androstenedione and estradiol appeared detrimental. In KGN cells, supraphysiological estradiol without androgen substrate suppressed downstream steroidogenesis, consistent with the adverse effects of excessive early estradiol exposure, supporting granulosa cell contribution to local androgen availability. - Source: PubMed
Sririwichitchai RungnapaSitticharoon ChantachaKeadkraichaiwat IssarawanMaikaew PailinChanheng SuchawadeePetyim Somsin - In brief: The RNA-binding protein Pumilio-2 (PUM2) is expressed by human granulosa cells and granulosa cell tumor cells, including KGN cells. Fundamental roles in the regulation of the innate immune abilities, proliferation, and steroidogenesis of KGN granulosa cells became apparent upon downregulation. Abstract: The RNA-binding protein Pumilio-2 (PUM2), encoded by PUM2, is known as a translational repressor with important roles -during embryonic development, cell differentiation, and synapse function. Information on its roles in the ovary were sparse, yet databank mining followed by immunohistochemistry revealed expression in nonhuman primate ovarian granulosa cells (GCs). Expression was also found in human in vitro fertilization-derived GCs, samples of human GC tumors (GCTs), and KGN cells, a well-established GCT-derived cell line. KGN cells were used to explore the roles of PUM2. A small interfering RNA (siRNA) targeting PUM2 reduced PUM2 levels in KGN cells, as seen in a proteomic analysis, which also revealed that a total of 51 -proteins were present at lower levels, while the abundance of 66 proteins was increased. Gene Ontology term analyses showed that the pathways mainly decreased were "response to virus," "defence response to virus," and "innate immune response." PUM2 may thus be a regulator of the innate immune abilities of GCs. The most increased pathway was "cell division," in line with increased proliferation of siRNA-transfected KGN cells. This underlies the increased ability to close the gap in scratch assays, as individual cell velocity or directionality of migration were comparable to controls. Downregulation of PUM2 also impaired the steroidogenic potential of KGN cells (lower HSD3B2 levels, lower progesterone in supernatant). Taken together, the results indicate fundamental roles of PUM2 not only in in the regulation of proliferation and steroidogenesis of human granulosa cells, but also in regulation of their innate immune abilities. - Source: PubMed
Eubler KatjaHerrmann CarolaScholz LinaJiang YuhaoBerg UlrikeBerg DieterDissen Gregory AMayr DorisPeitzsch MirkoForné IgnasiMayerhofer Artur - Congenital Adrenal Hyperplasia (CAH) is a group of diseases with an autosomal recessive inheritance pattern, which are caused by a defect in the enzymes involved in steroidogenesis in the adrenal cortex. Depending on the enzyme block variant, the spectrum of clinical manifestations of CAH varies from mild symptoms to potentially fatal disorders. The review provides a detailed analysis of the six main forms of CAH (lipoid hyperplasia, HSD3B2, CYP17A1, CYP21A2, CYP11B1, POR) with an in-depth description of their molecular basis, pathogenesis, and clinical and laboratory manifestations. Particular attention is paid to modern methods of genetic diagnosis of CAH, including analysis of the highly homologous CYP21A2 locus, prenatal and preimplantation diagnosis. Not only modern approaches to replacement therapy are described in detail, but also promising methods of treatment: corticotropin-releasing hormone receptor antagonists, gene- and cellbased technologies. The study's strength lies in its comprehensive analysis of the disease, spanning fundamental research to practical patient management, as applied to the realities of clinical practice in Russia. - Source: PubMed
Publication date: 2026/05/20
Vorontsova M VKokorina T SNuralieva N FYukina M YuTroshina E AMelnichenko G AMokrysheva N G