NR2F2 antibody
- Known as:
- NR2F2 (anti-)
- Catalog number:
- orb100485
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- NR2F2 antibody
Related genes to: NR2F2 antibody
- Gene:
- NR2F2 NIH gene
- Name:
- nuclear receptor subfamily 2 group F member 2
- Previous symbol:
- ARP1, TFCOUP2
- Synonyms:
- COUP-TFII, COUPTFB, SVP40, NF-E3, COUPTF2
- Chromosome:
- 15q26.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-21
- Date modifiied:
- 2018-02-14
Related products to: NR2F2 antibody
Related articles to: NR2F2 antibody
- The bipotential gonad is the precursor to the ovary and testis. In mice, gonad differentiation is initiated by commitment of presupporting cells into testicular Sertoli cells or ovarian granulosa cells. While drives testis differentiation, upstream drivers of ovary fate are unclear. We identified binding sites for basic helix-loop-helix (bHLH) transcription factors (TFs) upstream of granulosa genes and sought to investigate whether bHLH TFs regulate granulosa specification. bHLH transcription factor 4 (TCF4) was expressed in presupporting cells before sex determination. As development progressed, TCF4 was maintained in granulosa cells but lost in Sertoli cells. In mutant mice lacking the TCF4 DNA-binding domain, FOXL2 was reduced in granulosa cells and nuclear morphology was altered. Mutant ovaries failed to undergo morphological changes similar to wild-type littermates. Meanwhile, mutant testes appeared normal. We found that TCF4 binds the Mediator complex to regulate expression of gonadal genes (, ) and granulosa-enriched genes including and In ex vivo gonad culture, inhibition of JUN activation led to decreased expression. These results support the hypothesis that TCF4 regulates an underlying gonadal program that primes the gonad toward a female fate and is silenced in Sertoli cells downstream from . - Source: PubMed
Publication date: 2026/07/17
O'Neil Eleanore VDupont Shannon MLiang HuanSingh RohitCapel Blanche - Is exome sequencing (ES) an efficient approach for simultaneous analysis of causative single gene defects and copy number variants (CNV) in unexplained premature ovarian insufficiency (POI)? - Source: PubMed
Publication date: 2026/06/17
Valkna AnuKikas TriinJakovlev ÜlleMõttus OliverDutta AvirupErlang KülliPunab MargusRull KristiinaLaan Maris - The detailed molecular mechanisms and disease risk factors for heart failure, especially in the Japanese population, remain to be identified. In this study, we developed a -omics approach integrating multi-omics data to explore potential disease risk factors on a genome-wide scale. We functionally annotated the single-nucleotide polymorphisms (SNPs) investigated in a Japanese heart failure genome-wide association study using the epigenome data of -regulatory elements and regulome data of the transcription factor-binding regions identified in vascular endothelial cells. - Source: PubMed
Publication date: 2026/06/22
Hamano MomokoNomura SeitaroIto KaoruNakato RyuichiroKomuro IsseiYamanishi Yoshihiro - Congenital heart disease (CHD) represents the most prevalent and life-threatening birth defect. The identification of underlying factors contributing to abnormal cardiac development can offer valuable insights for the comprehensive medical management of affected pediatric patients. This study aimed to investigate the role and underlying mechanisms of GATA3-AS1 in the progression of CHD. The proliferation ability and apoptosis level of AC16 cardiomyocytes overexpressing GATA3-AS1 were detected by CCK-8 assay and flow cytometry. The downstream target miRNAs and mRNAs of GATA3-AS1 were validated using qPCR and western blot to elucidate the GATA3-AS1-associated ceRNA regulatory network. The interaction between GATA3-AS1 and its downstream target genes was validated using the dual-luciferase reporter assay. Finally, the expression patterns of GATA3‑AS1 and its downstream target genes were validated in clinical samples. Cellular functional assays demonstrated that the overexpression of GATA3-AS1 significantly suppressed the proliferation of AC16 cardiomyocytes while inducing apoptosis in these cells. The qPCR analysis revealed that, in AC16 cells overexpressing GATA3-AS1, the expression levels of NR2F2 were significantly upregulated, whereas the expression levels of miR-149-3p and miR-6769b-5p were significantly downregulated. Additionally, Western blot analysis further validated the significant upregulation of NR2F2 protein expression. The dual-luciferase reporter gene assay confirmed that GATA3-AS1 regulated cellular biological behavior by competitively binding to miR-149-3p with NR2F2. Finally, qPCR confirmed that the expression of GATA3-AS1, miR-149-3p, and NR2F2 in clinical samples were consistent with cytological experiments. GATA3-AS1 regulates the proliferation and apoptosis of AC16 cells via the GATA3-AS1/has-miR-149-3p/NR2F2 axis, potentially contributing to the formulation of more personalized and effective medical management strategies for patients with CHD. - Source: PubMed
Publication date: 2026/07/08
Wang HuamingLin XiGu QiuyangXu XiangWei LinglinLiu Xinxiu - - Source: PubMed
Publication date: 2026/07/02
Ye QianLiu ZhenyiZhang YuanyuanQiao ChangGuo HaotongZhi YanZhang ChaohuiHu GeZhang TaoWu YouranZhang Qian