Ask about this productRelated genes to: HSD17B8 antibody
- Gene:
- HSD17B8 NIH gene
- Name:
- hydroxysteroid 17-beta dehydrogenase 8
- Previous symbol:
- FABGL
- Synonyms:
- HKE6, D6S2245E, RING2, KE6, H2-KE6, SDR30C1
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-26
- Date modifiied:
- 2016-10-05
Related products to: HSD17B8 antibody
Related articles to: HSD17B8 antibody
- : Glomerular diseases (GD) possess strong polygenic susceptibility, yet exact causal genes remain unclear because most variants identified by genome-wide association studies (GWAS) reside in non-coding regions. While transcriptome-wide association studies (TWAS) effectively decode complex traits, cross-tissue profiling for GD remains largely unexplored. Therefore, this study employs an integrative cross-tissue TWAS and Mendelian randomization framework to systematically identify and validate novel GD susceptibility genes. : We conducted a systematic cross-tissue TWAS integrating Genotype-Tissue Expression (GTEx) v8 eQTL data across 49 tissues. Candidate genes were nominated using five complementary frameworks (sparse canonical correlation analysis (sCCA), functional summary-based imputation (FUSION), fine-mapping of causal gene sets (FOCUS), summary-data-based Mendelian randomization (SMR), and multi-marker analysis of genomic annotation (MAGMA)). Findings were refined via Mendelian randomization (MR), pathway enrichment, protein interaction networks, and druggability profiling. : We identified 21 candidate susceptibility genes for GD, with 10 genes (, , , , , , , , , ) strongly supported by MR analysis. Notably, five of these MR-prioritized genes (, , , , and ) were previously unreported. Functionally, these prioritized genes are primarily involved in immune modulation, inflammation, and steroid metabolism. Furthermore, five genes (, , , and ) were identified as potentially druggable targets. : This first systematic cross-tissue TWAS of GD prioritizes a set of genetically supported susceptibility genes. By uncovering novel drivers and druggable proteins, this study advances the mechanistic understanding of GD and provides a foundation for future therapeutic development and precision nephrology. - Source: PubMed
Publication date: 2026/05/08
Mao LichaoXu LinhongZhu TongLiu XintongLi Zehua - The 17β-hydroxysteroid dehydrogenase (hsd17b) gene family plays a pivotal role in sex steroid metabolism and gonadal differentiation in teleosts; however, their evolutionary dynamics and regulatory mechanisms during sex reversal in the mandarin fish (Siniperca chuatsi) remain poorly understood. In this study, we identified ten hsd17b family members in the S. chuatsi genome. Structural and phylogenetic analyses revealed the conservation of the core SDR domain across all members, alongside significant structural divergence in hsd17b4, which uniquely fused with SCP2 and PLN domains, indicating a pleiotropic role in both steroidogenesis and peroxisomal lipid metabolism. Spatiotemporal expression profiling demonstrated pronounced subfunctionalization: hsd17b4 exhibited robust testis-biased expression during spermatogenesis, whereas hsd17b1 was transiently upregulated during critical windows of ovarian differentiation. Furthermore, exogenous hormone treatments (MT, ETO, and E1) successfully induced functional sex reversal, accompanied by profound transcriptional reprogramming. Notably, ETO- and MT-induced masculinization was driven by a synergistic metabolic shift within the gonads. This process involved the significant up-regulation of the core testis-associated gene (hsd17b4), coordinated with genes facilitating cholesterol biosynthesis (hsd17b7) and estrogen inactivation (hsd17b8), effectively suppressing the female steroidogenic network (hsd17b1, hsd17b12a). Conversely, E1-induced feminization repressed male-pathway genes and promoted hsd17b1 transcription. Taken together, our findings demonstrate that the transcriptional antagonism and synergistic metabolic coordination among hsd17b members constitute the core molecular underpinning of endocrine-induced sexual plasticity. This study provides crucial molecular insights and viable targets for sex control breeding in teleost aquaculture. - Source: PubMed
Publication date: 2026/04/30
Li WeibinLin ShengyueChen WeijianDeng ZiyanCai GuojunXie ZihangZhang YongqingYang HaiyingDeng BinhuaLi QiangHan Chong - The Chinese mitten crab (Eriocheir sinensis) displays significant sexual dimorphism, a trait with considerable economic impact. However, the molecular mechanisms underlying its sex determination remain largely unknown. Early larval development, encompassing profound physiological transformation, is hypothesized to be a critical window for sexual fate decision. Here, we conducted whole-transcriptome sequencing of three early larval stages (megalopa before and after desalination, and the first juvenile crab stage), and integrated the data with previously published adult gonad transcriptomes. This enabled the construction of a sex steroid hormone-related ceRNA network active throughout development. Within this network, we identified a central regulatory axis consisting of lnc1778, miR-381-y, and Estradiol 17-beta-dehydrogenase 8 (HSD17B8). Their ceRNA interaction was experimentally validated using dual-luciferase reporter assays and expression correlation analyses. Expression profiling across larval stages and adult tissues revealed dynamic and sexually dimorphic patterns in adult tissues. HSD17B8 and lnc1778 were positively co-expressed in both sexes, significant negative correlations between HSD17B8/lnc1778 and miR-381-y were observed only in females. Furthermore, in vitro functional assays demonstrated that HSD17B8 catalyzes the conversion of estradiol-17β (E2) to estrone (E1) and testosterone (T) to androstenedione (A4), using NAD as a coenzyme. Our findings reveal a novel lncRNA-mediated ceRNA regulatory mechanism that regulates sex steroid hormone metabolism during early development and plays a key role in gonadal differentiation in E. sinensis. This study provides fundamental insights into crab gonadal development and offering potential molecular targets for sex-controlled aquaculture. - Source: PubMed
Publication date: 2026/03/01
Zhao FengShi YaxuanKong XinyuanZhang KaiZhang CongYin ShaowuNing Xianhui - Atrazine, a widely used chlorotriazine herbicide, persists in aquatic environments and poses potential carcinogenic risks. While epidemiological studies link atrazine exposure to malignancies, its intrinsic molecular mechanisms across organ systems remain incompletely understood. This study employed integrated network toxicology and transcriptomic analyses to clarify atrazine-associated oncogenic pathways in liver hepatocellular carcinoma (LIHC), kidney renal clear cell carcinoma (KIRC), lung adenocarcinoma (LUAD), and sarcoma (SARC). Transcriptomic data from The Cancer Genome Atlas (TCGA) for these cancers were analyzed to identify atrazine-related genes. Protein-protein interaction networks were constructed and analyzed to identify hub genes. Functional enrichment, immune microenvironment analyses, and survival analysis were performed. Molecular docking validated atrazine-target binding, and independent datasets were used for hub gene expression and pan-cancer relevance validation. We identified 92 (LUAD), 136 (LIHC), 137 (KIRC), and 161 (SARC) atrazine-associated targets. Hub genes including CDC6, MCM5/7, UBE2C, FEN1, CDCA8, and VIM were differentially expressed across these cancers. Enrichment analyses revealed atrazine disruption of core pathways, including cell cycle progression and chromosomal instability, epithelial-mesenchymal transition, metabolic reprogramming, and senescence-associated secretory pathways. Molecular docking confirmed high-affinity binding between atrazine and key targets. Pan-cancer validation implicated these hub genes in multiple additional malignancies. Transcription factor analysis nominated HSD17B8 as a key regulatory node. This study demonstrates that atrazine promotes carcinogenesis by dysregulating conserved networks governing genomic stability, cell proliferation, metabolic adaptation, and immune microenvironment remodeling, providing a mechanistic framework linking aquatic atrazine exposure to multi-organ carcinogenesis and nominating HSD17B8-associated pathways for therapeutic intervention. These findings underscore the imperative for enhanced environmental monitoring of atrazine contamination. - Source: PubMed
Publication date: 2026/01/08
Chen XiZhang XiangxinTang PingShang YifengWang YaoyuYin ChangqingWang LianleiZhang QunyeLiu XinyuYang QingYang Liu - (forkhead box protein L2) is a transcription factor, its function and regulatory mechanism have been mainly studied in mammals; related research on marine invertebrates is still insufficient. It was found that oogenesis was affected, and even a small number of cells resembling spermatogonial morphology appeared in ovaries after the was knocked down through RNA interference (RNAi) technology in our laboratory previously. Based on previous research, this paper conducted transcriptome sequencing and differential expression analysis on the ovarian tissues between the experimental group (post-RNAi) and the control group (pre-RNAi) of , and used recombinant protein for antibody production in Chromatin Immunoprecipitation Sequencing (ChIP seq) experiments to comprehensively analyze the pathways and key genes regulated by during oogenesis. The results showed that in the RNAi experimental group, 389 genes were upregulated, and 1615 genes were downregulated. Among the differentially expressed genes (DEGs), the differential genes related to gender or gonadal development are relatively concentrated in physiological processes such as steroid hormone synthesis, spermatogenesis, gonadal development, and ovarian function maintenance, as well as the FoxO and estrogen signaling pathways. Combining transcriptome and ChIP-seq data, it was found that there were some genes related to sex gonadal development among genes which were directly regulated by FOXL2, such as , , , , , , , , , , , and . This study lays the foundation for a deeper understanding of the FOXL2's specific regulatory mechanism during oogenesis in scallops as a transcription factor. - Source: PubMed
Publication date: 2025/09/12
Liu XiaolingYun HanXing YanWang ShuoZhou XueyingZhang Jianbai