NR1I2 CMV Expression Vector
- Known as:
- NR1I2 cytomegalovirus Expression Vector
- Catalog number:
- ME0024
- Product Quantity:
- 15 ug
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- NR1I2 CMV Expression Vector
Related genes to: NR1I2 CMV Expression Vector
- Gene:
- NR1I2 NIH gene
- Name:
- nuclear receptor subfamily 1 group I member 2
- Previous symbol:
- -
- Synonyms:
- ONR1, PXR, BXR, SXR, PAR2
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-23
- Date modifiied:
- 2016-10-05
Related products to: NR1I2 CMV Expression Vector
Related articles to: NR1I2 CMV Expression Vector
- Rifampicin is known to induce clindamycin metabolism via CYP3A4/5, but the magnitude of this interaction varies greatly from one patient to another. Because this metabolic induction results from rifampicin activation of the nuclear pregnane X receptor (PXR), the genetic polymorphisms of its NR1I2 gene and that of CYP3A4/5 might predict the risk of clindamycin underdosage when combined with rifampicin. We therefore conducted a study to determine the possible influence of NR1I2 and CYP3A4/5 gene polymorphisms on baseline and rifampicin-induced clindamycin clearance. - Source: PubMed
Publication date: 2026/08/15
Zeller ValérieLu EstelleMimram LéoBrinis KamiliaKerroumi YounesArnoux ArmelleLoriot Marie-AnneNarjoz CélineJullien Vincent - Quinalphos pesticide (QP) exposure can lead to various human health effects, including anaemia, leucocytosis with neutrophilia, hepatic damage and oxidative stress. Acute poisoning symptoms include weakness, sweating, impaired vision and neurological distress. Additionally, neurological and reproductive abnormalities have been reported in specific exposure scenarios. This study identified 16 differentially expressed genes from clinical exposure research. Integrating omics data using network biology approaches has shown that QP significantly alters the expression of 16 genes predicted to be regulated by 26 transcription factors and 41 miRNAs. The molecular docking predicted AR, ESR1, NR1I2, ESR2, CYP19A1 and JUN to have the highest binding affinity with QP. Gene ontology analysis of the DEGs revealed enrichment in pathways related to genital development, oestrogen receptor signalling, prostate gland development and response to vitamin A. The three most influential pathways by these DEGs are detected with significant enrichment in diseases, and they are linked to Cytochrome P450, arranged by substrate type, nuclear receptor transcription pathway and SUMOylation of intracellular receptors. The analysis identified 1445 drugs for 15 genes for potential drug repurposing. The network was pruned by applying the threshold value 0.1 STITCH database and score value 0.1 of the DGIdb database, resulting in the identification of 446 drug (approved and non-approved) therapeutic targets. This analysis provides a comprehensive understanding of the mechanisms of QP-induced toxicity, focusing on humans, and underscores the need for further studies on exposure to QP, providing valuable insights for toxicological risk assessment and regulatory evaluation. - Source: PubMed
Choudhari Jyoti KantSahariah Biju PravaJayapal Anand KumarChoubey JyotsnaTripathi Abhishek - Palbociclib is the more extensively evaluated CDK4-6 inhibitor in term of safety, efficacy and sources of pharmacokinetic variability. However, real-life data on the correlation between palbociclib plasma concentration, drug-drug interactions, gene polymorphisms and efficacy remain scarce. We previously characterized the effects of co-medications (CYP3A4 and P-glycoprotein inhibitors and antacid drugs) on palbociclib plasma concentration, and here we wanted to identify factors that influence progression-free survival in the same cohort of patients. - Source: PubMed
Publication date: 2026/07/28
Leenhardt FannyJacot WilliamLellouche LionelGuiu SeverineViala MarieFirmin NellyPayen AlexandreMbatchi Litaty CFiteni FredericEvrard Alexandre - We evaluated the therapeutic effect of psoralidin combined with cisplatin in a mouse model of breast cancer by H&E, immunohistochemistry and TUNEL staining. Transcriptome analysis, bioinformatics analysis and molecular docking analysis were used to explore the mechanism of psoralidin and cisplatin in improving breast cancer. The results showed that psoralidin could synergistically enhance the inhibitory effect of cisplatin on the proliferation of 4T1 breast cancer cells, promote the apoptosis of 4T1 cells, increase DNA damage and ROS expression. It also inhibited the expression of breast cancer cell proliferation-related molecules and energy metabolism factors related to tumor cell growth. Psoralidin could also synergistically enhance its inhibitory effect on tumor growth in breast cancer mice. Further molecular docking analysis revealed that psoralidin enhanced the killing effect of cisplatin on tumor cells by binding to Nr1i2. These findings provide a clear scientific basis for the enhancement of anticancer sensitivity to cisplatin by psoralidin. - Source: PubMed
Publication date: 2026/06/24
Zhong MeigongWu MeimeiChen RuizhenHe JiadiQiu YulanHuang JingMai YanyangLu WenjieWu WantingZheng MingzhuHuang XiaoxueLing JieRen LiangliangLi MinxianLin PeifengChen MinliZhang QinTo KwanNinWang YuRen DongChai XingxingWang LiliXue ZhonglinZhang Xin - This study aimed to investigate the causal relationship and biological mechanism between oral contraceptives (OCs) and adverse pregnancy outcomes using Mendelian randomization (MR) methods. - Source: PubMed
Publication date: 2026/05/19
Liu PengfeiDang ChunxiaoLiu JinxingYu XiaoSun Zhengao