ERAB Blocking Peptide
- Known as:
- ERAB Blocking Peptide
- Catalog number:
- 33r-10688
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- ERAB Blocking Peptide
Related genes to: ERAB Blocking Peptide
- Gene:
- HSD17B10 NIH gene
- Name:
- hydroxysteroid 17-beta dehydrogenase 10
- Previous symbol:
- HADH2, MRXS10
- Synonyms:
- ERAB, MHBD, 17b-HSD10, ABAD, SDR5C1, MRPP2, CAMR
- Chromosome:
- Xp11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-25
- Date modifiied:
- 2019-04-23
Related products to: ERAB Blocking Peptide
Related articles to: ERAB Blocking Peptide
- HSD10 mitochondrial disease (HSD10MD) is a rare X-linked disorder caused by pathogenic variants in the gene, encoding the mitochondrial enzyme 17β-hydroxysteroid dehydrogenase type 10 (HSD10). This enzyme is crucial for isoleucine degradation, neuroactive steroid metabolism, and mitochondrial function. HSD10MD typically presents in infancy or early childhood with severe neurodevelopmental regression, seizures, and cardiomyopathy, often leading to early mortality. Adult cases are extremely rare, with milder phenotypes associated with somatic mosaicism. - Source: PubMed
Publication date: 2026/02/26
Khodawrdi AlyaaMekki ChadiaLunati-Rozie ArianeFunalot Benoît - Epitestosterone (epiT) is the isomer of the androgen testosterone. Historically, the role of epiT has remained unclear. Recently, it has been reported that epiT promotes nuclear androgen receptor (AR)-dependent prostate cancer cell proliferation. The gut bacterium Clostridium scindens VPI 12708 was shown to convert androstenedione (AD) to epiT over three decades ago. The bacterial enzymatic pathways involved in epiT formation have only recently been reported. The desF gene encodes 17α-hydroxysteroid dehydrogenase which converts AD to epiT using NADPH as a cofactor. In this study, we quantitatively characterized DesF kinetic parameters and substrate specificity. The results revealed that the optimal pH for the reductive reaction is 7.0, and for the oxidative reaction it is 7.5 and 8.0. The kinetic analysis showed that for the reductive reaction, the K was 8.1 ± 1.8 µM and the V was 6.4 ± 0.3 µmol·min·mg; for the oxidative direction, the K was 27.3 ± 3.3 µM and the V was 7.2 ± 0.3 µmol·min·mg. Moreover, the substrate specificity analysis revealed that 11-keto-AD is the most favourable substrate for DesF, and the 17-keto group of 11-keto-AD can be converted to the 17α-hydroxy group. The phylogenetic relation between DesF and other characterized hydroxysteroid dehydrogenases reveals common ancestry with human HSD17B10 and Eggerthella lenta 3β-HSDH. These results are a significant advance in understanding epiT formation by the gut microbiome. - Source: PubMed
Publication date: 2026/03/05
Wang TaojunBinion BriawnaAlves João M PRidlon Jason M - Silica nanoparticles (SiO NPs) are widely used in biomedical and industrial applications, raising concerns about chronic exposure effects. This study investigated the impact of 90-day oral SiO NP exposure on male reproductive function in Wistar rats (n = 6). In accordance with OECD 408 guidelines and our 14-day range-finding study, doses of 500, 1000, and 2000 mg/kg were selected, with 2000 mg/kg identified as the highest nontoxic level for sub-chronic exposure, and reproductive endpoints including hormone levels, sperm quality, and testicular histopathology were subsequently evaluated. Exposure resulted in significant dose-dependent reductions in body weight, food intake, reproductive organ weights, and serum hormone levels such as testosterone (T), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) (p < 0.001), accompanied by histopathological damage to testicular tissue. Sperm count, vitality, motility, and morphology were significantly and dose-dependently impaired. Enzymatic activities of testicular biomarkers-including acid phosphatase (ACP), glucose-6-phosphate dehydrogenase (G6PD), γ-glutamyl transferase (γ-GT), and succinate dehydrogenase (SDH) were significantly decreased (< 0.001), suggesting metabolic dysfunction. Real-time PCR analyses revealed downregulation of SF-1 and associated steroidogenic genes (HSD3B1, HSD17B10, StAR), which was associated with altered testosterone biosynthesis. The observed SF-1 downregulation was associated with altered steroidogenic regulation, possibly mediated through oxidative and endocrine stress pathways. This study highlights the importance of assessing the long-term safety of SiONPs and their impact on reproductive health, particularly in the context of SF-1-mediated mechanisms. - Source: PubMed
Publication date: 2026/03/05
Umapati YMalashetty Vijaykumar B - A series of novel naphthoquinone[2,3-d] thiazole derivatives were designed as 17β-HSD10 inhibitors. Compound 14 emerged as the lead candidate, demonstrating potent 17β-HSD10 inhibition (IC = 6.33 μM) and favorable blood-brain barrier permeability. Molecular docking confirmed key interactions between its core scaffold and the 17β-HSD10 catalytic triad. In APP/PS1 mice, compound 14 significantly improved cognitive function without affecting 17β-HSD10 protein levels. It functionally inhibited 17β-HSD10, leading to rescued mitochondrial function (24% reduction in ROS, 76% increase in ATP, suppressed cytochrome c release), attenuated CDK5/p25 activation and Tau hyperphosphorylation, restored BDNF levels (58% increase in cortex), and reduced Aβ plaque load by approximately two-thirds. These results establish compound 14 as a multi-target neuroprotective agent for AD, concurrently ameliorating mitochondrial impairment, Tau pathology, and Aβ deposition through functional inhibition of 17β-HSD10. - Source: PubMed
Publication date: 2026/02/22
Liu ErfengDao ShiyunCui ChaoHe WanqingZhang LijunTang Huang - Lower grade gliomas (LGGs) exhibit significant molecular and clinical heterogeneity, challenging accurate prognosis and treatment strategies based on current parameters. Alterations in fatty acid metabolism (FAM) have been implicated in tumor initiation, proliferation, and metastasis. This study investigates the role of FAM in LGGs to enhance patient management. - Source: PubMed
Publication date: 2025/12/29
Du FangfangGuo YangShi XiangyuLiu Xiaomin