Ask about this productRelated genes to: SULT1E1 Blocking Peptide
- Gene:
- SULT1E1 NIH gene
- Name:
- sulfotransferase family 1E member 1
- Previous symbol:
- STE
- Synonyms:
- EST
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-18
- Date modifiied:
- 2016-10-05
Related products to: SULT1E1 Blocking Peptide
Related articles to: SULT1E1 Blocking Peptide
- Hepatic sexual dimorphism is critical for maintaining sex-specific metabolic pathways and xenobiotic clearance. We have demonstrated that in fibroblast growth factor 15 (Fgf15) transgenic (Tg) mice, FGF15 overexpression significantly reduced bile acid (BA) levels and induced hepatic feminization in males, marked by a male-to-female shift in expression of the drug metabolizing enzymes. This feminization is linked to the disruption of pulsatile growth hormone (GH) secretion pattern and signaling. However, it remained unclear whether FGF15 overexpression broadly disrupts hepatic sexual dimorphism or specifically drives a directional feminization program independent of biological sex. In this study, we profiled the hepatic transcriptome of female Fgf15 Tg mice and replenished male Fgf15 Tg mice with exogenous, pulsatile GH to test to what degree changes in the GH axis maintain liver dimorphism under low BA conditions. Beyond suppressing BA synthesis and altering steroid metabolism, female Tg mice altered expression of genes in xenobiotic metabolism and detoxification pathways, suggesting that the FGF15/BA axis regulates xenobiotic processing in females as well. Notably, FGF15 overexpression further amplified the baseline female expression profile of drug-metabolizing enzymes, characterized by the upregulation of female-predominant genes (Cyp2b9, Cyp3a41, Sult1e1, and Ugt1a1) and the suppression of male-predominant genes (Cyp7b1, Cyp2d9, Hsd3b5, and Igf1). Furthermore, pulsatile GH replenishment in male Tg mice partially restored male-predominant gene expression patterns. Taken together, these findings demonstrate that overexpression of intestine-derived FGF15 drives the feminization of sexually dimorphic hepatic gene expression independent of biological sex, a process that is at least partially mediated by impaired GH signaling. SIGNIFICANCE STATEMENT: Fibroblast growth factor 15 (Fgf15) overexpression intensified hepatic feminization of drug-metabolizing enzyme expression in female Fgf15 transgenic mice, similar to male Fgf15 transgenic mice. Restoring growth hormone signaling partially rescued the male-predominant gene expression pattern in male Fgf15 transgenic mice. This indicates that disruptions to growth hormone pulsatility, alongside sustained hepatic signal transducer and activator of transcription 5 activation, contribute to FGF15-induced hepatic gene feminization. - Source: PubMed
Publication date: 2026/07/15
Dai ManyunShi HongBasaly VeroniaMeadows VikKong BoGuo Grace L - Sexual dimorphism is a fundamental feature of aging, yet the liver-centric mechanisms underlying sex-specific aging trajectories remain incompletely understood. SIRT6, a NAD-dependent deacetylase, is a master regulator of genome stability, metabolic homeostasis, and longevity. However, its cell-type- and sex-specific functions in aging have not been fully characterized. Here, we generated hepatocyte-specific knockout (HKO) mice of both sexes and evaluated longitudinal lifespan, comprehensive metabolic profiling, hepatic histopathology, and transcriptomic profiles. Female HKO mice exhibited an acceleration of aging and a 17.60% reduction in median lifespan, characterized by severe systemic gerometabolic decline, visceral adiposity, and advanced metabolic-associated fatty liver disease (MAFLD). In stark contrast, aged male HKO mice displayed an enhanced catabolic state and lipid-clearing phenotype via the compensatory reprogramming. Mechanistically, hepatic deficiency in females exclusively hyperactivated the expression of estrogen sulfotransferase SULT1E1, resulting in reduced circulating estradiol levels. This hormonal collapse triggered a self-amplifying pathological triad of de novo lipogenesis, genomic instability, and cellular senescence. Crucially, pharmacological SIRT6 activation using the small-molecule activator MDL-800 suppressed expression, restored estrogen homeostasis, and successfully rescued the gerometabolic phenotypes in aged female mice. Collectively, these findings demonstrate that hepatic SIRT6 regulates female lifespan and healthspan by safeguarding estrogen homeostasis, defining the druggable SIRT6-SULT1E1 axis as a sex-stratified therapeutic target against age-related metabolic decline. - Source: PubMed
Publication date: 2026/08/05
Liu YonghuiZhang ZiliangWang TingtingYang XiuyanZhang QiufenLiu XinyiLu XuefengZhang JianFeng Li - : Prostate cancer (PCa) remains a prevalent malignancy among men, often complicated by recurrence and unfavorable clinical outcomes. Consequently, precise risk stratification and timely clinical intervention are paramount. Initially, we delineated distinct expression profiles of histone modification regulators via unsupervised clustering, identifying PCa subtypes with divergent survival probabilities and biological phenotypes. Subsequently, we sought to develop a prognostic gene signature, derived from the transcriptomic variations among these regulator-defined subtypes, to predict outcomes in PCa patients following radical prostatectomy (RP). : Clinical and transcriptomic data from PCa cohorts were retrieved from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) repositories for comprehensive analysis. Subtypes driven by histone modification regulators were established using unsupervised consensus clustering, followed by in-depth characterization of their molecular features and associated pathways. A risk-scoring model was then developed to evaluate its prognostic efficacy in this patient population. : Stratification based on histone modification regulators yielded four distinct PCa subtypes exhibiting heterogeneous survival outcomes, functional pathways, and genomic mutational landscapes. Following rigorous feature selection, a 21-gene risk signature (HIS_score)-comprising MXD3, CCDC28B, COL11A2, SLC39A5, GPT, DNASE1L2, PIF1, KRTAP5-9, TTLL10, KRTAP5-1, KRTAP5-10, HAGHL, MSLNL, AMH, NKAIN4, CCDC114, SLC9A3, SULT1E1, ALB, SLC6A14, and RPE65-was constructed. Survival analyses demonstrated that patients assigned to the high HIS_score cohort experienced significantly worse clinical outcomes compared to their low-score counterparts. Furthermore, we integrated this signature into a novel clinical nomogram to facilitate individualized prognostic assessments. : Derived from transcriptomic disparities between extreme epigenetic subtypes, the HIS_score and its associated nomogram serve as robust prognostic instruments. These tools effectively encapsulate the downstream transcriptional sequelae of histone modification dysregulation, offering clinicians a valuable framework to accurately predict post-RP outcomes and expedite the formulation of personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/05/28
Gao JialinZhou XueeZuo ZetaoHong JiahongTan YanRong XiaoxiangZhou RuiHuang Zhenhua - Fibromyalgia is a chronic musculoskeletal condition characterized by widespread pain, fatigue, and emotional dysregulation, with unclear pathophysiological mechanisms. In this bioinformatics-based analysis, gene expression data and protein-protein interaction (PPI) network analysis were used to identify differentially expressed genes (DEGs) associated with fibromyalgia. Among the identified 1050 DEGs, three hub genes-AGT, SNCA, and EZH2 emerged as potential key regulators of fibromyalgia progression. AGT, a key component of the renin-angiotensin system, is involved in blood pressure regulation, electrolyte balance, and neuroinflammatory processes, which may contribute to fatigue and heightened pain sensitivity in fibromyalgia. SNCA plays a role in synaptic dysfunction and central sensitization, key features of fibromyalgia's pain mechanisms. EZH2, an epigenetic regulator, modulates gene expression related to pain sensitization and neuroinflammation, emphasizing its significance in chronic pain pathways. These hub genes showed associations with pain targets, including BDNF, TAC1, and NGF, indicating their potential involvement in fibromyalgia-associated pain. Interactions with neuropathic pain genes in key brain regions-mPFC, NAc, and PAG-were observed; however, these associations are inferred from existing literature and were not directly measured in the present study. Additionally, connections to stress-related hormones, such as cortisol, dopamine, and serotonin, suggest that hormone-related gene expression changes may be associated with fibromyalgia symptoms, particularly pain sensitivity and emotional dysregulation. The downregulation of ESR2 and ABHD2, alongside the upregulation of SULT1E1, indicates potential alterations in estrogen-related pathways, which may be relevant to symptom severity, particularly in postmenopausal women. These findings, consistent with existing literature, suggest that AGT, SNCA, and EZH2 may serve as potential therapeutic targets, with EZH2 highlighted as an epigenetic regulator, and may provide a basis for future therapeutic exploration in fibromyalgia. - Source: PubMed
Publication date: 2026/05/07
Gowri Gopal KRobi Linda SSherin D R - : Meningiomas, the most common primary intracranial tumors, are predominantly benign, but high-grade variants show marked aggressiveness, histo-molecular heterogeneity, and treatment resistance. Although the 2021 WHO CNS classification integrates molecular and histopathologic criteria, substantial inter- and intratumoral variability still limits prognostic accuracy and treatment effectiveness. The goal was to provide insight regarding the histo-molecular intratumoral heterogeneity (ITH) of meningioma and examine its clinical implications. : A narrative review was performed in accordance with PRISMA guidelines. PubMed and Google Scholar were screened for studies on "meningioma" and "intratumoral heterogeneity" published up to 28 July 2025. Eligible studies included original human research reporting histological or molecular heterogeneity with clinical relevance. : Eighteen studies comprising 2952 meningioma patients (mean age 59.4 ± 14.8 years, range 16-85) were included. Integrated cytogenetic, molecular, and spatial analyses, including FISH, karyotyping, scRNA-seq, CNV profiling, and spatial transcriptomics, revealed multilayered histo-molecular heterogeneity. Histologically, regional variations in morphology and proliferative index increased with tumor grade. Genomic diversity, marked by recurrent losses of 1p, 14q, and 22q and transcriptionally distinct subclones, defined a complex tumor architecture. Spatial and temporal analyses demonstrated subclonal expansion, stepwise clonal evolution, and therapy resistance, particularly in recurrent tumors. Functionally, SULT1E1 subclones and COL6A3-mediated macrophage-tumor interactions emerged as potential key drivers of malignancy, recurrence, and radioresistance. : Histo-molecular diversity underlies meningioma progression, recurrence, and therapeutic resistance. Standardization of ITH assessment, integration of AI-based spatial analytics, and the development of subclone-specific therapies are essential next steps toward advancing precision neuro-oncology. - Source: PubMed
Publication date: 2026/04/10
Bankole Nourou Dine AdeniranLe Van TuanKerherve LucMorlaix EdouardBellus Jean-FrançoisBelhajali KerimaLopez JulianDe Buck PierreHouidi Alia SaydaFarah WalidLleu MaximeBaland OlivierCao CathyEl Cadhi AhmedBeaurain JacquesPicart ThiebaudBerhouma Moncef