Ask about this productRelated genes to: NR1I3 Blocking Peptide
- Gene:
- NR1I3 NIH gene
- Name:
- nuclear receptor subfamily 1 group I member 3
- Previous symbol:
- -
- Synonyms:
- MB67, CAR1, CAR
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-23
- Date modifiied:
- 2015-11-18
Related products to: NR1I3 Blocking Peptide
Related articles to: NR1I3 Blocking Peptide
- Diethylene glycol dibenzoate (DEGDB), an emerging eco-friendly plasticizer, remains critically understudied with mechanistic and molecular-level evidence linking it to clear cell renal cell carcinoma (ccRCC) progression, representing a major knowledge gap. To fill this gap, we conducted a cross-scale investigation using network toxicology, WGCNA, machine learning, SHAP explainable modeling, and molecular docking as methodological tools to elucidate DEGDB‑induced ccRCC progression. By jointly mining the ChEMBL, PubChem, SwissADME, STRING, and GEO repositories, we rigorously distilled a high-confidence set of 42 target genes, among which TSHR, ADORA2B, ANPEP, CA9, CYP3A4, JUN, NR1I3, and PHGDH were highlighted. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses revealed that DEGDB may propel ccRCC progression by disrupting neuro-endocrine-immune network regulation, activating chemical carcinogenesis-related receptors, and perturbing metabolic-degradation pathways such as nitrogen metabolism and lysosomal signaling. Subsequently, 113 machine-learning algorithms were leveraged to construct predictive models, and SHAP-based interpretation pinpointed five core genes-CA9, NR1I3, PHGDH, GABRA2, and ANPEP. Validation against The Cancer Genome Atlas (TCGA) datasets demonstrated that CA9 exhibits marked expression divergence in ccRCC (box-plot analysis) and is strongly associated with unfavorable prognosis (Kaplan-Meier survival curves). Molecular-docking simulations further confirmed robust binding affinities between DEGDB and all five core target proteins (binding energies < -5 kcal/mol). In vitro assays additionally revealed that DEGDB significantly promotes 786-O and A498 proliferation and up-regulates CA9 protein expression. Collectively, our findings indicate that DEGDB accelerates ccRCC progression via the orchestrated modulation of cellular proliferation, disruption of neuro-endocrine-immune homeostasis, and activation of oncogenic receptors. This study provides a theoretical framework for assessing the environmentally relevant health risks posed by emerging plasticizers and for devising preventive strategies against DEGDB‑induced ccRCC under real‑world exposure scenarios. - Source: PubMed
Publication date: 2026/05/22
Yanping MaGuolin TianTao YangAngyang DuJiaxin LiBo TaoYajie LiYaodong JiaYuelong FengHao YangLihong NieRuining Zhao - Risk assessment and management of endogenous potentially toxic components are critical for promoting the rational clinical use of herbal medicines. However, most herbal medicines lack sufficient safety data in clinical, especially for those with multiple botanical sources. As a commonly used multi-botanical source herbal medicine, Uncariae Ramulus Cum Uncis-derived indole alkaloids (IA-URCU) are primarily responsible for its potential hepatotoxicity in clinical practice. Nevertheless, the underlying mechanism of URCU-induced hepatocyte injury remains unclear. - Source: PubMed
Publication date: 2026/04/06
Yang BinSun XueqianZhang XinyueWang ShuoWang YeWang YumingYang ShenshenShu LexinLi Yubo - Current in vitro protocols differentiating hepatocytes fail to activate mature metabolic genes, induce zone-specific phenotypes, and suppress fetal liver signatures. In this issue, Taguchi, Magalhães et al. used CRISPR-Cas9 screening in a mouse model of hepatic development to identify Nr1i3 and Nfix as regulators of hepatocyte maturation and zonation. - Source: PubMed
Stephan Tabea LHoodless Pamela A - Individual differences in immune responses to African swine fever virus (ASFV), whether induced by vaccination or natural infection, may be linked to genetic variation in the genes involved in antigen presentation. - Source: PubMed
Publication date: 2025/12/11
Zhang FanghongNiu SiqiFrancisco Alegria AgostinhoAnzol Beneque AlbertoYao MinLiu GuopinWang JianwuHuang Tinghua - The maturation of lineage-committed embryonic hepatocytes requires both the timed activation of metabolic gene regulatory networks (GRNs) and silencing of embryonic programs to achieve adult hepatic functions. However, in vitro derivation of mature hepatocytes remains imperfect, and key transcriptional regulators governing GRN rewiring during late development are still insufficiently defined. To address this, we generated a developmental reference atlas and employed a dCas9 activation screen with single-cell transcriptomics on primary mouse embryonic hepatocytes, enabling effect ranking among late-onset transcription regulators. We identify Nr1i3 as a potent inducer of pericentrally expressed metabolic genes and Nfix as a critical suppressor of embryonic and periportal signatures. Supplementing liver zonation patterning signals with these regulators further enhanced the expression of pericentrally zonated metabolic genes, emphasizing the importance of a microenvironment-targeted approach. Our screening and analysis therefore highlight regulatory mechanisms underlying organ maturation and offer general strategies for improving the functionality of in vitro-derived cells. - Source: PubMed
Publication date: 2025/11/20
Taguchi AtsuhiroMagalhães Alexandre PBolondi AdrianoLee Ming-KangKretzmer HeleneWittler LarsHnisz DenesMeissner Alexander