NR1H4 polyclonal antibody
- Known as:
- NR1H4 pab (anti-)
- Catalog number:
- PAB12369
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- NR1H4 polyclonal antibody
Related genes to: NR1H4 polyclonal 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 polyclonal antibody
Related articles to: NR1H4 polyclonal antibody
- Acute inflammatory challenge can impair intestinal barrier function and bile acid homeostasis in weaned piglets. Glutamate serves as an important energy substrate and functional amino acid for intestinal epithelial cells, yet the epitranscriptomic mechanisms underlying its potential protective effects remain poorly defined. This study investigated whether dietary glutamate supplementation is associated with mA-dependent regulation of SLC10A2 and bile acid signaling in weaned piglets subjected to an acute LPS challenge, with supporting validation in IPEC-J2 cells. LPS challenge (100 μg/kg body weight) impaired ileal morphological structure, activated the TLR4/NF-κB signaling pathway, and aggravated intestinal inflammatory responses in piglets. In contrast, glutamate supplementation was associated with restored ileal mucosal morphology, up-regulated expression of intestinal tight junction proteins, and suppressed TLR4/NF-κB pathway activation. Further metabolomic analysis indicated that LPS stimulation and glutamate intervention altered ileal bile acid metabolism: LPS decreased total bile acid (TBA) content in ileal tissue while increasing TBA accumulation in ileal chyme, whereas glutamate treatment partially reversed this pattern, by elevating ileal tissue TBA and reducing chyme TBA, suggesting a facilitatory effect of glutamate on intestinal bile acid reabsorption. Glutamate supplementation was also associated with increased ileal ASBT (SLC10A2) and FXR (NR1H4) expression. The SLC10A2 transcript exhibited detectable mA modification; glutamate supplementation rescued the LPS-induced downregulation of mA demethylases FTO and ALKBH5, which was associated with reduced global and SLC10A2-specific mA modification. In vitro experiments in IPEC-J2 cells suggested that inhibition of FTO or glutamate dehydrogenase attenuated the effects of glutamate on mA modification and SLC10A2 expression, and that YTHDF2 may contribute to the degradation of hyper-mA-modified SLC10A2 mRNA. Glutamate-derived α-KG may serve as a cofactor supporting demethylase expression and activity after LPS stimulation. Collectively, these findings suggest that glutamate may alleviate LPS-induced intestinal inflammation in weaned piglets through a pathway involving α-KG-dependent maintenance of mA demethylase expression, reduced mA modification of SLC10A2, and preserved ASBT/FXR signaling. This study provides evidence for a nutritional-epitranscriptomic axis that may contribute to intestinal protection under acute inflammatory stress. - Source: PubMed
Publication date: 2026/09/10
Gan ZhendingHe JiaweiJin QiyueMa QiuqinWang ChuanlongZhong Xiang - 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