NR2F6 antibody - middle region (ARP32995_T100)
- Known as:
- NR2F6 (anti-) - middle region (ARP32995_T100)
- Catalog number:
- arp32995_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NR2F6 antibody - middle region (ARP32995_T100)
Related genes to: NR2F6 antibody - middle region (ARP32995_T100)
- Gene:
- NR2F6 NIH gene
- Name:
- nuclear receptor subfamily 2 group F member 6
- Previous symbol:
- ERBAL2
- Synonyms:
- EAR-2, EAR2
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1989-02-23
- Date modifiied:
- 2018-02-14
Related products to: NR2F6 antibody - middle region (ARP32995_T100)
Related articles to: NR2F6 antibody - middle region (ARP32995_T100)
- - Source: PubMed
Publication date: 2026/04/09
Klepsch VictoriaWolf DominikBaier Gottfried - Valproic acid (VPA) is an antiepileptic drug associated with hepatic steatosis, yet the transcriptional regulators determining cellular susceptibility to VPA remain incompletely defined. In a time-series RNA-sequencing analysis of primary human liver spheroids, NR2F6 emerged as one of the nuclear regulators predicted to shape the hepatocellular response to VPA. In parallel, a shRNA screen targeting 42 nuclear receptors in HepG2 cells independently identified NR2F6 as a sensitizer of VPA toxicity. Functional validation in HepG2 and HepaRG models demonstrated that NR2F6 knockdown significantly increased VPA-induced lipid accumulation, whereas lipid accumulation triggered by oleic and palmitic acid remained unaffected, indicating a VPA-specific steatogenic vulnerability. To characterize NR2F6-dependent transcriptional programs, we performed RNA-sequencing in shNR2F6 and shGFP HepaRG cells exposed to VPA for 72 h. Although VPA was the principal driver of transcriptional variance, reduced NR2F6 expression markedly amplified the VPA-induced transcriptomic response. shNR2F6 cells exhibited coordinated upregulation of nuclear-encoded oxidative phosphorylation genes across Complexes I, III, IV, and V, while mitochondrial genome-encoded subunits remained unchanged, suggesting nuclear-driven mitochondrial compensation. NR2F6 knockdown also altered key lipid-associated pathways, including reduced induction of CPT1A and exaggerated induction of PLIN2, linking NR2F6 deficiency to impaired fatty-acid import and enhanced lipid-droplet accumulation. Together, these results identify NR2F6 as a key modulator of hepatocellular adaptation to VPA, linking nuclear receptor signaling to mitochondrial and lipid-metabolic remodeling and revealing a previously unrecognized regulatory node in drug-induced steatosis. - Source: PubMed
Publication date: 2026/04/03
Guo KaidiVerheijen Marchavan Herwijnen MarcelCaiment Florianvan den Beucken Twan - belong to the superfamily of ligand-dependent transcription factors that act as sensors for hormones, vitamins and dietary lipids. are differentially expressed in normal mammary and breast-cancer tissues. Unlike other , lack known physiological ligands. Limited information is available on function in breast-cancer. - Source: PubMed
Publication date: 2026/03/09
Caricasulo Maria AzzurraParoni GabrielaZanetti AdrianaBrunelli LauraKurosaki MamiCavallaro Andrea VincenzoFoglia MarikaRemoli GabriellaGuarrera LucaBolis MarcoTerao MinekoGarattini Enrico - CAR-T cell therapy is effective in hematologic malignancies but remains challenging in solid tumors owing to antigen heterogeneity and tumor microenvironment-induced exhaustion. Here, gene editing of the nuclear receptor NR2F6 restores CAR-T cell functionality, sustaining a TCF1⁺ progenitor-exhausted phenotype, enhancing metabolic fitness, and preserving cytotoxic potency under chronic antigen exposure. In immunocompetent models, Nr2f6-deficient CAR-T cells suppress solid tumor growth and induce robust, polyclonal host antitumor responses that persist after CAR-T clearance, as demonstrated by tumor re-challenge protection. Although infused CAR-T cells disappear within 2 weeks, durable tumor control coincides with epitope spreading and secondary immune responses, likely via dendritic cell reactivation. Protection against antigen-negative tumors and transferable immunity reveal a dual mode of direct cytotoxicity followed by durable immune reprogramming. This broadened host immunity may offset immune escape driven by antigen heterogeneity or loss, establishing NR2F6 inhibition as a promising CAR-T engineering strategy for durable, antigen-agnostic solid-tumor immunotherapy. - Source: PubMed
Publication date: 2026/02/27
Humer DominikKlepsch VictoriaRieder DietmarHölzl IsabelSchreiber DanielLang ViktorKoutník JiříPeer SebastianSajinovic TajanaWille VianaFürst AnnaSavic DraganaDiem GabrielPosch WilfriedSkvortsova Ira-IdaKrogsdam AnneSopper SieghartKobold SebastianTrajanoski ZlatkoSiegmund KerstinThuille NikolausGruber ThomasWolf DominikBaier Gottfried - Diet-induced metabolic disorder is a global health concern, and bioactive polysaccharides have been shown to mitigate metabolic disorder by modifying gut microbiota. Polysaccharides from Schizophyllum commune have shown excellent anti-obesity effects, but the specific regulatory mechanisms remain unclear. Herein, we reported that SCP could effectively inhibit 3 T3-L1 preadipocyte differentiation in vitro and supplementation with SCP alleviated obesity in HFD-fed mice. SCP treatment significantly enriched Faecalibaculum rodentium and ILA and increased the expression levels of several lipid metabolism-related genes including AMPKα, PGC-1α and PPARγ. The anti-obesogenic effects of SCP can be transferred by FMT. SCP supplementation and FMT significantly increased the ILA levels in serum and feces. Moreover, FMT significantly increased the levels of miR-144-5p, miR-142a-5p and miR-150-5p; these miRNAs were enriched in the phosphatidylinositol signaling pathway and were positively correlated with the content of ILA. The lipogenesis-related gene Nr2F6 was coregulated by the above miRNAs, and its expression level significantly increased in FMT mice. These results indicate that SCP ameliorates diet-induced obesity by increasing the abundance of F. rodentium and ILA as well as the expression levels of certain miRNAs. Our study may provide a new reference for understanding the anti-obesogenic effects of natural polysaccharides. - Source: PubMed
Publication date: 2025/09/24
Yin ChaominLi ChenFan XiuzhiShi DefangLi JiangtaoQiu JianhuiYao FenYu WeiGao Hong