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
- 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 - The constitutive androstane receptor (CAR, NR1I3) has been recognised as a nuclear receptor for various xenobiotics, such as barbiturates and dietary polyphenols. In this study, the CAR responded to internal metabolites produced by intestinal bacteria from the dietary amino acid tryptophan. We screened 15 indole-containing compounds in HepG2 cells using a luciferase reporter assay and found that three of them, tryptamine, indole-3-pyruvic acid, and indole-3-ethanol, significantly increased transcriptional activity of both mouse and human CAR. The estimated EC values of these compounds at the micromolar concentration order, which were close to those found in the host sera and tissues. Importantly, 3-methyl indole (skatole) inhibited mouse CAR activity to a lesser extent than androstanol, an inverse agonist of mouse CAR. Considering this, we investigated the transactivation mechanisms of these compounds in terms of their nuclear translocation. Indole-3-pyruvic acid and diindolylmethane slightly but not significantly increased the nuclear translocation of mouse CAR, whereas skatole significantly increased nuclear translocation. This is in contrast to the observation that androstanol does not induce nuclear translocation. Tryptamine is produced by Ruminococcus gnavus and skatole by Lactobacillus spp. Our findings suggest that the CAR can be positively or negatively regulated by indole-containing metabolites, depending on the composition of the gut microbiota. - Source: PubMed
Publication date: 2025/09/12
Narita RyuyaKaito MisakiKondo TakashiAbe KeikoYasuoka Akihito