Nr1h4
- Known as:
- Nr1h4
- Catalog number:
- 043760A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Nr1h4
Related genes to: Nr1h4
- 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
anti-Bile Acid Receptor NR1H4anti-Bile Acid Receptor NR1H4anti-Bile Acid Receptor NR1H4 (1B10)anti-Bile Acid Receptor NR1H4 (1B10)anti-Bile Acid Receptor NR1H4 type: Primary antibodies host: Mouseanti-NR1H4 (1G11)anti-NR1H4 (1G11), Mouse monoclonal to NR1H4, Isotype IgG1, Host Mouseanti-NR1H4(1G11)anti-NR1H4(1G11) type: Primary antibodies host: MouseBovine Bile acid receptor(NR1H4) ELISA kitBovine Bile acid receptor(NR1H4) ELISA kitBovine Bile acid receptor(NR1H4) ELISA kit SpeciesBovineBovine nuclear receptor subfamily 1, group H, member 4 (NR1H4) ELISA kitBovine nuclear receptor subfamily 1, group H, member 4 (NR1H4) ELISA kit, Species Bovine, Sample Type serum, plasmaCanine Bile acid receptor(NR1H4) ELISA kit Related articles to: Nr1h4
- 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, NR1H4) and G-protein-coupled bile acid receptor 1 (TGR5, GPBAR1), 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 MadsHinrichs Gitte RyeSvenningsen 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 - Gastrointestinal stromal tumors (GIST) can become malignant upon recurrence and metastasis, yet no drugs specifically target these processes. This study explores the effectiveness and mechanism of paeoniflorin in treating GIST. Initially, the impact of paeoniflorin on the viability, proliferation, and migration of GIST cell lines (GIST-T1 and GIST-882) was assessed using CCK-8, transwell, and wound healing assays at low (5 μM) and high (20 μM) concentrations. Subsequently, datasets GSE136755 and GSE21315 were analyzed to identify potential therapeutic targets for inhibiting GIST transfer. Key genes and pathways related to Paeoniflorin's anti-GIST effects were identified through molecular docking and Western blotting. Paeoniflorin influenced cell viability, proliferation, and migration in GIST-T1 and GIST-882 cell lines at low (5 μM) and high (20 μM) concentrations. We identified 761 differentially expressed genes (DEGs) and selected 50 hub genes using a PPI network. By screening paeoniflorin's potential targets, we identified eight key genes (CYP1A2, CYP2C9, CYP3A4, F2, ICAM1, NR1H4, PLG, and SERPINE1) that were significantly elevated in metastatic GIST samples. CYP3A4 was confirmed as a target of Paeoniflorin in GIST treatment through molecular docking and Western blotting. Pan-cancer analysis showed CYP3A4's enrichment in the tight junction pathway and a significant negative correlation with AKT2 protein. Paeoniflorin treatment led to high AKT2 expression in the tight junction pathway in GIST cell lines. Paeoniflorin acts on the CYP3A4 protein to affect the tight junction pathway, inhibiting the malignant metastasis of GIST. - Source: PubMed
Publication date: 2026/04/23
Cui DapengCui ZeyinLi YansenFan ShuangLi LeiYang ChengYu RuixiaCui JiaxinFu RunjiaFei Jiandong