EAR2 _ NR2F6
- Known as:
- EAR2 _ NR2F6
- Catalog number:
- Y213147
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- EAR2 _ NR2F6
Related genes to: EAR2 _ 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: EAR2 _ NR2F6
anti-NR2F6anti-NR2F6anti-NR2F6anti-NR2F6anti-NR2F6 type: Primary antibodies host: MouseChicken EAR2 (Eosinophil Associated Ribonuclease A family Member 2) ELISA KitChicken EAR2 (Eosinophil Associated Ribonuclease A family Member 2) ELISA KitCOUP transcription factor 3,COUP-TF3,Ear2,EAR-2,Ear-2,Erbal2,Mouse,Mus musculus,Nr2f6,Nuclear receptor subfamily 2 group F member 6,V-erbA-related protein 2COUPg,Ear2,EAR-2,Erbal2,Nr2f6,Nuclear receptor subfamily 2 group F member 6,Ovalbumin upstream promoter gamma nuclear receptor,Rat,Rattus norvegicus,V-erbA-related protein 2Ear2EAR2 NR2F6 Immunizing PeptideEAR2 (anti human nuclear recepter antibody, cloneH9929A)EAR2 (anti human nuclear recepter antibody, cloneH9929A)EAR2 (anti human nuclear recepter antibody, cloneN2025)EAR2 (anti human nuclear recepter antibody, cloneN2025) Related articles to: EAR2 _ NR2F6
- Hepatitis C virus (HCV) infection frequently progresses to chronicity, where persistent antigen exposure drives differentiation of virus-specific CD8+ T cells toward an exhausted phenotype. This state is defined by progressive upregulation of inhibitory receptors and functional impairment of antigen-specific T cells. Because patients span distinct clinical stages from acute infection to spontaneous resolution or therapy induced sustained virological response, HCV provides a unique model to study how T-cell exhaustion is established, maintained, and potentially reversed. While PD1 and TIGIT are well established in this context, CD96 (TACTILE) is a less-characterized receptor that shares its ligand CD155 with TIGIT and DNAM-1 and may modulate CD8+ T-cell differentiation and function. - Source: PubMed
Publication date: 2026/07/13
Knapp MaximilianAckermann ChristinWittner MelanieBeisel ClaudiaCords LeonWestphal TimLam LizKummer SilkeWoost RobinPeine SvenPischke SvenSchultheiß ChristophLohse Ansgar WWalker AndreasTimm JörgBinder MaschaSchulze Zur Wiesch Julian - 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