Mouse Monoclonal to NR2F6
- Known as:
- Mouse Monoclonal NR2F6
- Catalog number:
- 11-719-c025
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Exbio praha a.s.
- Gene target:
- Mouse Monoclonal NR2F6
Related genes to: Mouse Monoclonal to NR2F6
- 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: Mouse Monoclonal to NR2F6
Related articles to: Mouse Monoclonal to NR2F6
- Gliomas represent the most prevalent and aggressive primary brain tumors in adults. Accumulating data suggest a strong connection between mitochondrial dysfunction and cancer development. However, signature markers for assessing mitochondrial genetic risk in human glioma remain limited. This study aims to identify mitochondrial genes associated with glioma patient prognosis, develop a strong mitochondrial-related gene signature (MRGS), and analyze the tumor immune microenvironment (TIME) related to this signature. The expression profiles and prognostic value of MRGS were analyzed using R language, GraphPad Prism 8 and online databases. - Source: PubMed
Publication date: 2026/06/23
Harmak ZakiaNaji OumaymaBaddi HamzaGhazi BouchraBadou Abdallah - - 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.Trial Registration 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 - BACKGROUND: Orphan-Nuclear-Receptors belong to the Nuclear-Receptors superfamily of ligand-dependent transcription factors that act as sensors for hormones, vitamins and dietary lipids. Orphan-Nuclear-Receptors are differentially expressed in normal mammary and breast-cancer tissues. Unlike other Nuclear-Receptors, Orphan-Nuclear-Receptors lack known physiological ligands. Limited information is available on Orphan-Nuclear-Receptors function in breast-cancer. METHODS: We performed a number of silencing studies based on the use of siRNAs targeting the Orphan-Nuclear-Receptors expressed in a panel of cell-lines, recapitulating breast-cancer heterogeneity. NR2F6 function was further validated by stable shRNA-mediated silencing in estrogen-receptor-positive (MCF7) and triple-negative (MDA-MB-231) cell-lines. This was followed by assays on proliferation, clonogenicity and motility in MCF7 and MDA-MB-231 cells as well as cytokine responses in MCF7 cells. Whole-genome RNA sequencing was used to define NR2F6-dependent transcriptional networks. Immunoprecipitation coupled with flow-injection high-resolution mass-spectrometry was performed to identify endogenous molecules binding NR2F6. RESULTS: Significant levels of ten Orphan-Nuclear-Receptors were observed in most breast-cancer cell-lines and in mammary tumor tissues. Functional siRNA studies revealed that NR2F2 and NR4A2 silencing enhanced the proliferation of breast-cancer cells, indicating a potential tumor-suppressive role. In contrast, NR2F6 knockdown consistently reduced proliferation of breast-cancer cells, supporting an oncogenic role. NR2F6 is highly expressed in breast tumors as compared with their normal counterparts. Stable NR2F6 silencing decreased the growth and clonogenicity of MCF7 and MDA-MB-231 cell lines, corroborating the siRNA findings. In the mesenchymal and high motility MDA-MB-231 cell-line, NR2F6 silencing diminished directional cell migration. In the epithelial MCF7 cell-line, this Orphan-Nuclear-Receptor induced an antiproliferative response to immune cytokines. From a mechanistic point of view, NR2F6 knock-down up-regulated gene-networks related to cell-cell and cell–matrix interactions, while it down-regulated gene-networks involved in cell-cycle progression and proliferation. A mass-spectrometry–based ligand screening approach led to the identification of palmitoylethanolamide as the only endogenous molecule capable of binding NR2F6 with high-affinity. CONCLUSION: Our study identifies NR2F6 as an oncogenic driver of breast-cancer and a promising therapeutic target for the personalized treatment of this tumor. The discovery of palmitoylethanolamide as a physiological ligand of NR2F6 provides the molecular foundation for a rational design of NR2F6 antagonists/inhibitors to be evaluated for their therapeutic potential 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