Ask about this productRelated genes to: NR2F6 Blocking Peptide
- 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 Blocking Peptide
Related articles to: NR2F6 Blocking Peptide
- - 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 - The connection between immunity and Parkinson’s disease (PD) is well-established. Myeloid immune responses influence the microenvironment of the central nervous system (CNS), which can be modulated by sargramostim, a recombinant granulocyte-macrophage colony-stimulating factor (GM-CSF). Previous studies have demonstrated sargramostim’s neuroprotective effects, which are linked to its safety and tolerability, as well as its ability to regulate innate immunity. Changes in myeloid biomarkers correlate with clinical responses. PD symptoms were assessed using the Unified PD Rating Scale (UPDRS). Ten subjects received sargramostim through subcutaneous injections of 3 µg/kg, administered five days every week. Myeloid biomarkers were measured before treatment and at six and twelve months of treatment. Protein expression by Western blotting and gene expression by transcriptomic analysis was correlated with UPDRS III scores. Recognizing the exploratory nature of this study, patient responses were classified into potent, moderate, or no change groups based on UPDRS III score reductions of 9–13, 5–7, or none, respectively. Biomarkers from all 10 patients identified FOXP3 as a “potential” signature biomarker. The potent responders showed biomarkers linked to autophagy, inflammatory, and antioxidant proteins, including ATG7, HMOX1, RELA, and TLR8. Moderate responders displayed biomarkers associated with RELA and LRRK2. Transcriptomic analysis revealed over 2000 differentially expressed anti-inflammatory, calcium-binding, and epigenetic genes. Among these, genes such as ANXA9, CALM3, CY7B1, HDAC4, HMGB2, NR2F6, PDIA3, REST, SACS and SOX4 were identified as potential predictors of changes in UPDRS III scores. Baseline levels of ATG7, CARD9, and SACS may serve as initial biomarkers to identify subjects likely to respond to sargramostim. Female patients exhibited unique UPDRS III scores in response to sargramostim treatment. Novel cell-based biomarker signatures were identified that may predict responses to sargramostim treatment in this hypothesis-generating study. We acknowledge the inherent study limitations by limited patient numbers. This was reflected in the comparisons offered for the patient sub-groups in the year-long trial. The trial is registered on ClinicalTrials.gov under identifier NCT03790670, dated 01.30.2019. - Source: PubMed
Publication date: 2026/04/01
Sil SusmitaDu XiaoqingAkter SamiaKumar MohitOludipe Davina BSaha ArnabHu GuokuOstlund Katie RHaynatzki Gleb RSantamaria PamelaMosley R LeeGendelman Howard E - 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