Ask about this productRelated genes to: HSD11B1 antibody
- Gene:
- HSD11B1 NIH gene
- Name:
- hydroxysteroid 11-beta dehydrogenase 1
- Previous symbol:
- HSD11B, HSD11
- Synonyms:
- SDR26C1
- Chromosome:
- 1q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-11-14
- Date modifiied:
- 2016-10-05
Related products to: HSD11B1 antibody
Related articles to: HSD11B1 antibody
- Prenatal hypoxia is a clinically relevant adverse factor that may affect fetal development both directly and through activation of maternal glucocorticoid signaling. The placenta plays a central role in this process by regulating fetal exposure to maternal glucocorticoids, yet it remains unclear whether hypoxia-induced endocrine alterations can extend into the next generation and modify placental and fetal brain glucocorticoid regulation during embryogenesis. Here, we investigated whether maternal hypoxia programs the glucocorticoid phenotype of adult female offspring and whether this phenotype is associated with altered placental glucocorticoid signaling and fetal brain corticosterone exposure in their progeny. - Source: PubMed
Publication date: 2026/08/24
Potapova SofiyaTyulkova EkaterinaVetrovoy Oleg - Enterobacterial infections being severe, with a high mortality rate, particularly affecting ICU patients, and 80% newborns. These infections have multifactorial multi-drug resistance (MDR) mechanisms, which frequently causes current antibiotic therapies to fail, mortality rate remains high, and creating an urgent need for alternative multi-targeted therapies, such as plant-derived compounds to restore clinical effectiveness. This study aims to discover novel anti enteric compounds in Hydrocotyle javanica Thunb. (H. javanica) belongs to Apiaceae family and understanding their interaction mechanism with enterobacterial infection targeted genes, using network pharmacology with in-silico docking and molecular dynamics simulation approaches. Four bioactive compounds as tetracosanoic acid, alpha-Amyrenyl acetate, stigmasterol glucoside, stigmasterol were identified as potential therapeutic agents. Most of the compounds exhibited favourable pharmacokinetic properties, complying with Lipinski's rule, with high bioavailability score 0.85 and non-toxic profiles. In-silico antibacterial prediction indicated both bacterial and bacteriostatic activities. A total of 53 common targets were identified with network analysis revealing key hub genes including HSD11B1, PTGS2,FDFT1,CYPHA1, and AKR1C2. Functional enrichment analysis showed significant involvement in immune and inflammatory pathways, particularly calcium signaling, MAPK signaling and reactive oxygen species related pathways. The docking result showed highest binding affinity, with stigmasterol showing highest score (-10.7 kcal/mol). A 100 ns molecular dynamics simulation further confirmed the stability of the stigmasterol-protein complex, with stable RMSD values 1-2 Å, low RMSF fluctuations and consistent hydrogen bonding, indicating sustained structural integrity. The present study highlights that phytocompounds from Hydrocotyle javanica exhibit significant binding affinity toward key enterobacterial targets, along with favorable ADME and toxicity profiles. These findings suggest their potential as promising lead molecules for anti-enterobacterial drug development, warranting further experimental validation. - Source: PubMed
Publication date: 2026/08/20
Paul DebasmitaGhosh MeghaMandal Manab - Taraxasterol (TAR) exerts therapeutic effects on various liver diseases via its inherent hepatoprotective and anti-inflammatory properties. However, the mechanism by which TAR treats hepatic fibrosis remains unclear. This study aims to identify the potential targets and specific molecular mechanisms underlying the therapeutic effects of TAR on hepatic fibrosis. DDC- and CCl -induced mouse models of hepatic fibrosis are established. The human hepatic stellate cell (HSC) line LX-2 and primary mouse HSCs are used for experiments. Transcriptomics, network pharmacology, single-cell transcriptomics, and molecular docking are employed to identify potential therapeutic targets of TAR for hepatic fibrosis. Functional validation is performed via HSD11B1 overexpression and knockdown experiments, and the regulatory role of the ERK MAPK pathway is verified using the specific inhibitor U0126. Histological staining results show that TAR significantly alleviates DDC- and CCl -induced hepatic fibrosis in mice and reduces associated liver injury. assays reveal that TAR effectively reverses TGF-β-induced activation of LX-2 cells and primary mouse HSCs. Multi-omics and docking analyses identify HSD11B1 as a direct target of TAR, whose downregulation in activated HSCs is restored by TAR treatment. Functional experiments demonstrate that overexpression of HSD11B1 attenuates TGF-β-induced HSC activation, while knockdown abolishes the therapeutic effects of TAR. Subsequent transcriptomic analysis confirms that HSD11B1 suppresses the ERK MAPK pathway, and knockdown of compromises the therapeutic efficacy of the ERK MAPK inhibitor U0126. In summary, TAR alleviates liver fibrosis by inhibiting HSC activation through the HSD11B1-ERK MAPK axis. - Source: PubMed
Publication date: 2026/08/03
Wang PengZhou HaoxiongDing YumingChen YanLiu HuilingJiang JieWu Bin - Non-small cell lung cancer (NSCLC) is the predominant subtype of lung malignancy. Accumulating epidemiological evidence demonstrates that environmental lead (Pb) exposure as a critical driver of its initiation and progression. - Source: PubMed
Publication date: 2026/07/30
Xu YinlanDong JieLiu HejunZheng JinmeiGuo HaonanChen YueWang JialinWu Weidong - While magnesium isoglycyrrhizinate (MgIG) is a clinically approved therapy for alcohol-associated liver disease (ALD), its precise molecular targets and mechanisms remain uncharacterized. This study aimed to define MgIG's hepatoprotective actions in chronic-binge ALD mouse models and ethanol/palmitic acid-exposed AML-12 hepatocytes. Through an integrated strategy encompassing RNA sequencing, molecular docking, and microscale thermophoresis, we discovered that MgIG directly binds to hydroxysteroid 11-beta dehydrogenase 1 (HSD11B1) at residue 187, a finding corroborated by molecular dynamics simulations. In vivo, MgIG markedly attenuated alcohol-induced liver injury, evidenced by ameliorated histological damage, reduced hepatic steatosis, and normalized liver-to-body weight ratios. In vitro, it effectively reduced lipid accumulation, inflammation, and apoptosis. Mechanistically, RNA sequencing identified isopentenyl diphosphate delta isomerase 1 (IDI1) as a key downstream effector. Hepatocyte-specific genetic manipulations confirmed that MgIG modulates the SREBP2-IDI1 axis, thereby suppressing lipogenesis, inflammatory responses, and apoptotic pathways. We reveal HSD11B1 as a novel direct molecular target of MgIG and elucidate its therapeutic mechanism through the HSD11B1-SREBP2-IDI1 signaling axis, which profoundly impacts ALD pathogenesis. These findings not only validate MgIG's clinical utility but also highlight a promising new therapeutic target for ALD. - Source: PubMed
Publication date: 2026/07/28
Xiao LuLi LuWu ShashaChe ZhaoyiDu YuyangZheng JingyiYan JingsongWang HaoZhang HongLi YanXiao Jia