NR1H4 Antibody
- Known as:
- NR1H4 Antibody
- Catalog number:
- GWB-68D503
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- NR1H4 Antibody
Related genes to: NR1H4 Antibody
- Gene:
- NR1H4 NIH gene
- Name:
- nuclear receptor subfamily 1 group H member 4
- Previous symbol:
- -
- Synonyms:
- FXR, RIP14, HRR1, HRR-1
- Chromosome:
- 12q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-17
- Date modifiied:
- 2018-03-06
Related products to: NR1H4 Antibody
Related articles to: NR1H4 Antibody
- 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 - Edema formation and ascites are common features in liver disease. The excessive accumulation of body water is caused by increased kidney water retention; yet the mechanisms linking liver and kidney function remain incompletely understood. This review explores the emerging concept of a liver-kidney axis, with bile acids (BAs) as potential mediators for kidney water handling. In cholestatic liver disease, as seen in liver cirrhosis, impaired hepatic BA flow to the duodenum elevates systemic BA concentrations, which can modulate signaling pathways through the BA receptors Farnesoid X receptor (FXR, ) and G-protein-coupled bile acid receptor 1 (TGR5, ), thereby increasing kidney Na and water retention in experimental models. Moreover, BAs can directly activate the sodium channel ENaC in isolated mouse collecting ducts and in mouse distal colon epithelial cells. Thus, BAs can promote sodium and water retention in parallel with the classical sodium- and water-retaining systems, such as the renin-angiotensin-aldosterone system. This effect may potentially contribute to water retention in pregnancy-associated conditions and in proteinuric kidney diseases, where liver function is affected, e.g., by loss of plasma proteins, altering hepatic BA metabolism. In this review, we will describe the synthesis of BAs, their modifications, and kidney BA metabolism in health and disease, and highlight a potential dynamic interplay between liver and kidney function, mediated in part by BAs, with implications for understanding and treating water retention disorders. - Source: PubMed
Publication date: 2026/06/09
Lynggaard Elkjær AmandaSkov Jensen IbenGabriel Tiddy MadsRye Hinrichs GitteSvenningsen Per - IgA nephropathy (IgAN) is a common glomerulonephrites worldwide. We herein aimed to investigate the pathogenic mechanisms underlying IgAN and to identify hub targets. The IgAN-related datasets were derived from the Gene Expression Omnibus database. Hub targets were identified by integrating differentially expressed gene (DEG) analysis and multiple protein-protein interaction (PPI) network algorithms. Functional enrichment and immune landscape analyses were conducted to explore the functional impacts of the hub targets. An IgAN cell model was employed to confirm the hub gene expression and its effect on cell proliferation in vitro. Drugs targeting the hub gene were validated via molecular docking. By integrating DEG and multiple PPI network algorithms, NR1H4 was significantly downregulated in IgAN comparing to control samples, which was successfully validated in multiple datasets, clinical cohort, and IgAN cell model. A total of 48 pathways were significantly enriched in both NR1H4 low vs. high expression groups and IgAN vs. control groups. Moreover, NR1H4 overexpression significantly inhibited the abnormal cell proliferation of IgA1-induced HMCs in vitro. NR1H4 showed great clinical potential in IgAN, particularly in terms of diagnostic value (AUC > 0.7) and as a drug target (e.g., the promising drug like obeticholic acid). In conclusion, NR1H4 downregulation probably contributed to the development of IgAN by promoting abnormal cell proliferation, highlighting its considerable clinical potential in the management strategy of IgAN. - Source: PubMed
Publication date: 2026/05/09
Li XianYang WenSun Changxi - To explore the clinical, genetic, treatment and prognostic characteristics of progressive familial intrahepatic cholestasis type 5 (PFIC5). - Source: PubMed
Dong MengjunXia ZhiyiLi SuliZhao YanbingZhou Fang - This study investigated the effects and underlying mechanisms of a fructo-oligosaccharide (FOS) and sea buckthorn complex (FS) on blood glucose and lipid metabolism in type 2 diabetic mellitus (T2DM) rats. The T2DM model was induced by a high-fat diet (HFD) combined with alloxan administration. Prior to rat experiments, the synergistic hypoglycemic and hypolipidemic effects of FOS and sea buckthorn have been verified by zebrafish experiments. FS intervention significantly reduced fasting blood glucose, triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) in rats, although high-density lipoprotein cholesterol (HDL-C) showed a non-significant increasing trend. 16S rDNA sequencing revealed that FS significantly reshaped gut microbiota; it enriched beneficial genera (, , ) and suppressed inflammation-associated taxa (, -). Transcriptomic analysis indicated that FS reversed aberrant expression of inflammation-related genes (, , , in the colon) and metabolism-related genes (, , in the liver), activating pathways including fat digestion and absorption and fatty acid metabolism, while inhibiting immune-inflammatory pathways (, the "TNF signaling pathway", "Th17 cell differentiation"). Serum bile acid (BA) profiling showed FS modulated levels of primary and secondary BAs ( CA, α-MCA, HDCA, GHDCA), restoring metabolic homeostasis. Pearson correlation analyses demonstrated robust associations among key microbiota, BAs, blood glucose/lipid indices, and farnesoid X receptor (FXR/) expression, supporting a regulatory network involving the gut-liver axis. This study elucidates the multi-target mechanisms by which FS ameliorates glucolipid metabolic disorders in T2DM, gut microbiota remodeling, attenuation of intestinal/hepatic inflammation, and BA metabolism crosstalk, providing a theoretical basis for prebiotic-based precision nutrition. - Source: PubMed
Publication date: 2026/05/26
Chen LingLiu HualinChen YanwuXiao QianyaHuang ZijinLi ZiyingZhang XiaofeiFan XueyingXiao MeichenLi XiaominChen Yuan Yao