NR1H4 protein - N_A Polyclonal
- Known as:
- NR1H4 protein - N_A Polyclonal
- Catalog number:
- 18-003-42422
- Product Quantity:
- 0.05 mg Aff Pur
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- NR1H4 protein - N_A Polyclonal
Related genes to: NR1H4 protein - N_A Polyclonal
- 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 protein - N_A Polyclonal
Related articles to: NR1H4 protein - N_A Polyclonal
- The ubiquitous tire-derived pollutant 6PPD-quinone (6PPD-Q) poses potential systemic health risks, yet its toxicological impact on the intestinal tract, particularly in the context of ulcerative colitis (UC), remains largely unknown. This study aimed to investigate whether 6PPD-Q aggravates DSS-induced colitis and to identify candidate molecular events using integrative computational and experimental approaches. - Source: PubMed
Publication date: 2026/08/31
Li JingyiGao XizhuangXu YeminWang LuZhu YingDeng Bin - In the present study, we report the effects of soy protein concentrate (SPC) on growth parameters, liver morphology and hepatic transcriptomic response on totoaba (Totoaba macdonaldi) (153 ± 0.84 g). Two experimental isoenergetic diets (IDs), each containing 44% protein and 11% lipids, were formulated by replacing 30% (SPC30) and 60% (SPC60) of fish meal with SPC and compared to a commercial diet (CD) containing fishmeal. Treatments were performed in triplicate (n = 12 per replicate) over a period of 90 days. Fish fed the CD or SPC30 diets showed no significant differences in final weight (fW: 618.4 ± 20.13 and 624.4 ± 16.97 respectively). Conversely, fish fed the SPC60 diet exhibited the lowest growth performance (fW: 260.10 ± 57.65 g, weight gained: 68.84 ± 0.94 g and specific growth rate: 0.36 ± 0.22%). Liver from totoaba fed the CD showed a typical, uniform hepatic organization. In contrast, livers from SPC30 and SPC60 groups displayed lipid vacuole infiltration in hepatocytes and central displacement of the nuclei. Functional gene enrichment analysis of transcripts revealed that biological processes (BP), such as protein catabolism (ctra, ctrb, ela1, cbpb1, cbpa1), stress responses (bfar, dab, casp8, pawr), anatomical structure development (stml2, lrig2, hgf, ret), bile acid biosynthesis (s27a2, ntcp7, nr1h4) and lipid transport (s27a2, lipe4, fabpi), were the molecular mechanisms most affected by SPC supplementation. Collectively, these BPs suggest negative effects of SPC60 supplementation in totoaba. - Source: PubMed
Publication date: 2026/09/12
Larios-Soriano ErnestoLópez-Galindo Laura LCarrillo Roberto AAcuña Lus M LópezMendoza-Porras OmarGalaviz Mario A - N- (1,3-Dimethylbutyl)-N'-phenyl-p-phenylenediamine quinone (6PPD-Q), a tire rubber antioxidant derivative, accumulates in air, soil, and water and has been found in urine, blood, and cerebrospinal fluid, posing significant health risks. Although 6PPD-Q exhibits intestinal toxicity, its role in inflammatory bowel disease (IBD) remains unclear. The objective of this study was to identify key molecular targets of 6PPD-Q in IBD and to validate their involvement in 6PPD-Q-induced intestinal epithelial cell injury. Using network toxicology, machine learning, molecular docking, and in vitro experiments in human intestinal epithelial cells, we identified 60 overlapping 6PPD-Q-IBD targets, enriched in lipid metabolism, oxidative stress, and inflammation. Multi-model machine learning screened six core genes (NR1H4, ANXA5, SPARC, PCK1, PDK2, and CFB), with NR1H4 as a key mediator. Molecular docking showed strong binding of 6PPD-Q to NR1H4, exceeding that of its parent compound. In vitro experiments confirmed that 6PPD-Q caused lipid droplet and cholesterol accumulation, mitochondrial dysfunction (manifested as ATP synthesis inhibition, mitochondrial ROS burst, decreased membrane potential, and mitochondrial fragmentation), and significantly upregulated the levels of pro-inflammatory cytokines IL-6, TNF-α, and IL-8, thereby triggering inflammatory responses. Moreover, 6PPD-Q exposure significantly downregulated NR1H4 expression. These findings reveal that 6PPD-Q increases IBD risk by interfering with lipid metabolism, disrupting mitochondrial function, upregulating inflammatory cytokines, and downregulating NR1H4, providing important evidence for understanding the risk posed by this emerging environmental pollutant to IBD and for developing preventive strategies. - Source: PubMed
Publication date: 2026/09/04
Wu PeiwenHu WeibinChen GangZhao XuZhang Xiaozhi - (Bai-zhi) and (Dang-gui) are traditional food-medicines used for skin disorders, but the mechanism of their oral efficacy remains unclear. Probiotic fermentation is a promising strategy to enhance the bioactivity of plant-based foods. - Source: PubMed
Publication date: 2026/08/18
Li YuyuanXiang DandanHuang XingdaLi JixiangDu XuxuYuan DonglinHou ChenglongWang QianWu YuanhangHou BinbinWang ChaoranRen YixinLi Ming - : The clinical management of visceral pain remains a significant challenge. Our previous study confirmed the analgesic efficacy of dexmedetomidine (Dex) in a mouse model of inflammatory visceral pain (IVP). However, the underlying molecular mechanism, particularly regarding immune regulation, has not been fully elucidated. : In the present study, transcriptomic profiling of both physiological and disease states was performed to characterize associated molecular and immune signatures. Key driver genes were identified by integrating differentially expressed genes (DEGs) from the IVP model with potential Dex targets derived from network pharmacology. Molecular docking simulations evaluated binding interactions. The correlations between Dex's targets and immune cell infiltration patterns, with a focus on macrophages, were analyzed. : Multi-tissue analysis revealed a strong association between IVP pathogenesis and pro-inflammatory immune responses, specifically a shift in macrophage polarization. Within this dysregulated network, seven proteins were identified as direct potential targets of Dex. Among these, six core targets, such as ADGRF1, IDO1, JAK3 and NR1H4, demonstrated the most significant correlations with M1-like macrophages and exhibited strong in silico binding potential with Dex. : This integrated analysis suggests that Dex may alleviate visceral pain by modulating a specific gene network linked to pro-inflammatory macrophage activation, thereby promoting the restoration of immune balance. Our findings provide a novel mechanism-informed perspective for the application of Dex in visceral pain therapy. - Source: PubMed
Publication date: 2026/08/10
Ke PengLi YuyingLiu FengQiu LiangchengWu HanWu Xiaodan