NR1H4 antibody - middle region (ARP33672_P050)
- Known as:
- NR1H4 (anti-) - middle region (ARP33672_P050)
- Catalog number:
- arp33672_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NR1H4 antibody - middle region (ARP33672_P050)
Related genes to: NR1H4 antibody - middle region (ARP33672_P050)
- 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 - middle region (ARP33672_P050)
Related articles to: NR1H4 antibody - middle region (ARP33672_P050)
- Yifei Sanjie Formula (YFSJF), a traditional Chinese medicine (TCM) formulation, has been clinically observed to enhance the efficacy of programmed cell death protein 1 (PD-1) blockade in patients with advanced lung adenocarcinoma. However, the underlying mechanisms of its effect remain unclear. This study aimed to clarify the molecular mechanism by which YFSJF enhances the efficacy of PD-1 inhibitors, with a focus on its role in regulating the ubiquitin-specific protease 7 (USP7)-nuclear receptor subfamily 1 group H member 4 (NR1H4)-bile acid metabolism axis. - Source: PubMed
Publication date: 2026/03/11
Ren YangziLi YuanliangFang ChongkaiChen ZhiqiangXiao Zhiwei - Loss-of-function mutations in bile acid (BA)-activated farnesoid x receptor (FXR/NR1H4) cause severe neonatal liver pathology in humans, earlier referred to as progressive familial intrahepatic cholestasis type 5 (PFIC5). However, Fxr-deficient mice do not develop early-onset liver disease, possibly due to the predominance of hydrophilic muricholic acids (MCAs) in their BA pool. Mice lacking Cyp2c70 display a human-like BA composition, lacking MCAs. This study aimed to evaluate whether Fxr/Cyp2c70-double knockout (DKO) mice recapitulate the pathophysiology of human FXR-deficiency. - Source: PubMed
de Vries Hilde DLi JinxiaoUstyantsev KirillHovingh Milaine VMulder Niels LHavinga RickPalmiotti Annade Bruyn KrisztinaAttema BrechtWeersing EllenThomas Rachel EBloks Vincent WBerezikov Eugenevan Faassen MartijnVerkade Henkjan Jde Boer Jan FrearkKuipers Folkert - Understanding the molecular determinants of interindividual drug response variability remains a major challenge in pharmacogenomics. Very Important Pharmacogenes (VIPs), as defined by PharmGKB, represent genes with well-established roles in drug metabolism and efficacy. However, their activity occurs within complex molecular networks that extend beyond direct pharmacogenetic associations. We constructed a VIP-centered subnetwork and applied network topology analyses, including shortest path, signal propagation, and degree centrality, to identify key nodes mediating VIP interactions. Functional enrichment, transcription factor (TF) association, and drug-gene interaction analyses were subsequently performed to characterize the biological and pharmacological context of these networks. Our results revealed a dense VIP interactome enriched in metabolic, endocrine, and signaling pathways. Notably, we identified a subset of highly connected non-VIP genes that frequently bridge canonical VIPs, termed shadow VIPs. These genes, often encoding transcriptional regulators, such as , , and , and more frequent in the shortest paths connecting VIPs, such as POR, APP, and GIPC1, exhibited strong associations with approved drugs, particularly hormone-related and antineoplastic agents. This suggests that shadow VIPs may act as indirect regulators of pharmacogenomic phenotypes by influencing the expression or activity of canonical VIPs. Additionally, the analysis revealed that shadow VIPs, on average, exhibit lower RVIS values than VIPs, indicating a higher intolerance to functional mutations. This suggests that shadow VIPs are under stronger selective selection, underscoring their essential biological roles. Together, these findings expand the current pharmacogenomic framework, demonstrating that drug response mechanisms emerge from a wider network of regulatory and functional interactions. Introducing the concept of shadow VIPs highlights new molecular candidates for pharmacogenetic exploration and emphasizes the value of network-based approaches in advancing precision medicine. - Source: PubMed
Publication date: 2026/03/19
de Melo Nicolly ClementeAccioli Guilherme SilvaSánchez-Luquez KarenGomes Mateus Freitas de FariasFelicio Aline Cristinade Carvalho Lucas Miguel - Acetaminophen (APAP)-induced hepatotoxicity represents a critical medical emergency due to the rapid progression. To date, practical and feasible early interventions are limited. This study aimed to explore whether farnesoid X receptor (FXR, NR1H4) alleviates APAP-induced acute liver injury and whether this effect is mediated by fibroblast growth factor 2 (FGF2) activation to promote liver regeneration. - Source: PubMed
Publication date: 2026/03/29
Wang RuiChen JiaqiWang WenyuLi XiaXiao YatingShi YuboQv YifanWang ChangyuanFu TingMeng Qiang - Glyphosate, one of the most widely used herbicides worldwide, has raised significant concerns regarding its potential involvement in hepatotoxicity and molecular changes associated with liver cancer biology. These concerns highlight the need to better understand its underlying molecular mechanisms in hepatoma cells. Emerging evidence suggests that glyphosate exposure may increase the risk of liver cancer and chronic liver disease. However, the precise molecular alterations and promising biomarkers associated with glyphosate-induced hepatic toxicity and disease remain largely unexplored. In this study, an RNA-Seq-based in silico systems biology approach was employed to elucidate glyphosate-induced differential transcriptional profiling in hepatoma cells. This analysis revealed significant transcriptional profiling characterized by the upregulated hub genes and . These genes were primarily associated with glucose metabolism, TNF-α/NF-κB signaling, epithelial-mesenchymal transition (EMT) and cellular stress responses. Conversely, several key genes were significantly downregulated, including , , , , , , , , and , which were involved in lipid metabolism, immune regulation and non-alcoholic fatty liver disease (NAFLD) pathways. Notably, all hub genes demonstrated strong diagnostic performance, highlighting their potential as sensitive biomarkers of glyphosate exposure. Collectively, this study provides comprehensive insights into gene expression changes associated with glyphosate exposure in hepatoma cells, linking them to hepatic metabolic dysregulation and immune modulation and suggesting a panel of hub genes with potential diagnostic and therapeutic significance. - Source: PubMed
Publication date: 2026/03/19
Mishra Divya