NR0B2 is an unusual orphan receptor that contains a putative ligand-binding domain but lacks a conventional DNA-binding domain. It is a member of the nuclear hormone receptor family, a group of transc
- Known as:
- NR0B2 unusual orphan receptor contains a putative ligand-binding domain lacks a conventional Desoxyribonucleic acid-binding domain. a member nuclear hormone receptor family, a family transc
- Catalog number:
- 25-311
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- NR0B2 unusual orphan receptor that contains putative ligand-binding domain but lacks conventional DNA-binding domain. member the nuclear hormone family group transc
Related genes to: NR0B2 is an unusual orphan receptor that contains a putative ligand-binding domain but lacks a conventional DNA-binding domain. It is a member of the nuclear hormone receptor family, a group of transc
- Gene:
- NR0B2 NIH gene
- Name:
- nuclear receptor subfamily 0 group B member 2
- Previous symbol:
- -
- Synonyms:
- SHP
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-19
- Date modifiied:
- 2016-10-05
Related products to: NR0B2 is an unusual orphan receptor that contains a putative ligand-binding domain but lacks a conventional DNA-binding domain. It is a member of the nuclear hormone receptor family, a group of transc
Related articles to: NR0B2 is an unusual orphan receptor that contains a putative ligand-binding domain but lacks a conventional DNA-binding domain. It is a member of the nuclear hormone receptor family, a group of transc
- is an edible medicinal fungus with potential metabolic benefits, but its effects on type 2 diabetes mellitus accompanied by hyperlipidaemia (T2DM-HLP) remain incompletely understood. This study evaluated the effects of orally administered ethanol extract (EAE; 2.0 g kg) and cordycepin (50 or 100 mg kg) in a T2DM-HLP mouse model over 6 weeks. Metabolic indices, serum transaminases, colon and liver histology, gut bacterial and fungal communities, serum metabolites, and FXR/TGR5-related molecular markers were assessed. Compared with the model group, EAE and 50 mg kg cordycepin reduced serum lipid and transaminase levels to varying degrees and were associated with downward shifts in fasting blood glucose and oral glucose tolerance test curves. Histological alterations in the colon and liver were also less apparent in these two groups. Faecal 16S rDNA and ITS sequencing showed changes in the bacterial and fungal community structure, while untargeted serum metabolomics identified distinct metabolic profiles involving bile acids, fatty acids, amino acids, nucleotides, and redox-related metabolites. Enrichment analyses implicated bile secretion, primary bile acid biosynthesis, cholesterol metabolism, cAMP signalling, and amino acid metabolism. These changes were accompanied by increased colonic TGR5 and hepatic FXR immunoreactivity, increased hepatic , , and expression, and reduced expression. Responses to 100 mg kg cordycepin were less consistent, indicating no simple dose-dependent relationship under the present conditions. Overall, EAE and cordycepin were associated with improved metabolic status and coordinated changes in the gut microbial composition, serum metabolism, and bile acid-related molecular readouts. - Source: PubMed
Publication date: 2026/09/21
Shi HuaijieMeng YingZhang GuoyingLing Jianya - The enterohepatic bile acid system undergoes profound developmental and adaptive changes that remain incompletely defined. Here, we profiled bile acid metabolism genes across hepatic ontogeny, tissue distribution, acute fasted-refed, and four chronic MASH models. Classic bile acid synthesis genes were activated in a perinatal-to-weaning wave, with the FXR-SHP feedback loop being functional from birth. In adults, synthesis and FXR-SHP regulation were strictly hepatic, while active reabsorption and FGF15 signaling were ileal, establishing clear spatial compartmentalization. Acute fasting revealed metabolic flexibility, with Shp elevation persisting even after Fxr had returned to baseline. In chronic MASH, this flexibility was lost in a model-specific manner, ranging from FXR-SHP uncoupling to transcriptional collapse. These findings establish that the bile acid metabolic program is precisely wired across development and space, flexibly tuned to acute nutritional status, and progressively dismantled under chronic metabolic injury-a transition that may represent an early event in MASH pathogenesis. - Source: PubMed
Publication date: 2026/07/09
Lin HaiyueYe JingjingBai Qiufang - Food-responsive enteropathy (FRE) is a common form of chronic inflammatory enteropathy in dogs. Its underlying molecular mechanisms remain incompletely characterized. Increasing evidence from human studies and emerging canine data suggests that bile acids (BAs) influence intestinal homeostasis and inflammation. Duodenal mucosal biopsies from dogs with FRE ( = 8) and healthy controls ( = 4) were analyzed by bulk RNA sequencing. Differential expression analysis (DESeq2), KEGG and Reactome pathway enrichment, and GSEA were performed with a specific focus on BA transport, sensing, and metabolic pathways. FRE samples showed a distinct BA-associated transcriptional signature, including a non-significant decreasing trend of the BA receptor NR1H4 (FXR) expression (padj = 0.057), and significant upregulation of the nuclear receptor RXRA, together with increased expression of downstream mediators NR0B2 (SHP) and FGF19. BA transport components such as SLC51A (OSTα) and ABCC3 (MRP3) were differentially regulated, and the BA-synthetic enzyme HSD3B7 was increased. Bile secretion was among the top enriched KEGG pathways (ranked 9th; NES = 1.935; padj = 0.005). This study provides, to our knowledge, the first focused mucosal transcriptomic evidence of coordinated BA-axis alterations in canine FRE. The findings align with mechanisms described in human inflammatory bowel disease and support further investigation of bile acid signaling in canine chronic enteropathy. Findings should be interpreted as exploratory due to cohort heterogeneity. - Source: PubMed
Publication date: 2026/06/11
Mózes BorbálaKiss GergelyFóthi ÁbelFerenczi SzilamérPsáder Roland - Anthocyanins are plant polyphenols widely regarded as antioxidants, yet they can exert concentration-dependent effects and act as pro-oxidants in specific contexts. Although their protective role in stressed testicular cells is established, their impact on Leydig cell steroidogenesis under non-pathological conditions remains poorly understood. Here, we investigated how an anthocyanin-enriched fraction from (0-1.00 μg/mL) affects androgen synthesis in murine TM3 Leydig cells. Cell viability, intracellular ROS, antioxidant capacity, mitochondrial function, androstenedione production, steroidogenic gene expression, and the exometabolome by H-NMR were assessed. The fraction exhibited biphasic, dose-dependent effects. At 0.01 μg/mL, it induced a mitohormetic response, upregulating mitochondrial complexes III and V. Conversely, higher concentrations (0.10-1.00 μg/mL) reduced metabolic activity, increased intracellular ROS, and significantly suppressed androstenedione synthesis independently of . These concentrations also induced dose-dependent repression of , concomitant with upregulation of , encoding the transcriptional repressor Small Heterodimer Partner (SHP). Overall, the data support a redox-dependent mechanism whereby elevated ROS promotes expression, leading to suppression and impaired androstenedione production. These findings challenge the view of anthocyanins as uniformly beneficial for male fertility and identify as a sustainable source of bioactive anthocyanins capable of modulating redox-endocrine homeostasis in a dose-dependent manner under basal conditions. - Source: PubMed
Publication date: 2026/04/23
Patanè Giuseppe TMoreira Ruben JMartins Ana DOliveira Pedro FPutaggio StefanoBarreca DavideAlves Marco G - T-2 toxin is a highly toxic mycotoxin commonly present in food and the environment, with accumulating evidence supporting its hepatotoxic potential. However, the molecular events linking T-2 toxin exposure to liver fibrosis remain insufficiently characterized. - Source: PubMed
Publication date: 2026/05/20
Qiao LichunShi ShaotengWang LiangjiaShafiq Muhammad AftabTang JingLi MiaoqianWan PingZhou JingxuanDai XuleiHan JingGuo Yijie