FOXC1 antibody - N-terminal region (ARP38036_P050)
- Known as:
- FOXC1 (anti-) - N-terminal region (ARP38036_P050)
- Catalog number:
- arp38036_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FOXC1 antibody - N-terminal region (ARP38036_P050)
Related genes to: FOXC1 antibody - N-terminal region (ARP38036_P050)
- Gene:
- FOXC1 NIH gene
- Name:
- forkhead box C1
- Previous symbol:
- FKHL7, IRID1
- Synonyms:
- FREAC3, ARA, IGDA, IHG1
- Chromosome:
- 6p25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-06-05
- Date modifiied:
- 2019-04-23
Related products to: FOXC1 antibody - N-terminal region (ARP38036_P050)
Related articles to: FOXC1 antibody - N-terminal region (ARP38036_P050)
- Peritumoral brain edema (PTBE) is an important prognostic factor in meningiomas and may persist after tumor resection. While clinical and radiological predictors of postoperative PTBE resolution are known, the impact of molecular markers remained unclear. The aim of this study was to investigate the association of Forkhead box C1 (FOXC1) expression, as well as radiological and clinical parameters with postoperative PTBE resolution. - Source: PubMed
Publication date: 2026/06/11
Basaran Alim EmreBraune MaxBarrantes-Freer AlonsoMüller Wolf CVychopen MartinGüresir ErdemWach Johannes - To evaluate long-term visual outcomes in Axenfeld-Rieger Syndrome (ARS), quantify blindness rates, and identify risk factors of blindness in ARS-related glaucoma. - Source: PubMed
Publication date: 2026/06/09
Seresirikachorn KasemThiamthat WarakornBitrian ElenaCheng Ta Chen Peter - How systemic hormonal signals coordinate stem cell fate decisions in adult tissues remains incompletely understood. In bone marrow, Cxcl12-abundant reticular (CAR) cells, marked by Early B-cell Factor 3 (Ebf3) expression, are multipotent mesenchymal progenitors that maintain the hematopoietic stem cell niche and serves as a major osteoblast progenitor source during adult bone remodeling. Using inducible lineage tracing coupled with single-cell transcriptomics and conditional genetics in mice, we show that intermittent parathyroid hormone (iPTH; teriparatide) drives osteogenesis from CAR cells by simultaneously engaging cell-intrinsic and cell-extrinsic mechanisms. Directly, iPTH suppresses lineage-enforcing transcription factors Ebf3, Ebf1, and Foxc1, thereby destabilizing progenitor identity and priming CAR cells for osteogenic commitment. Simultaneously, iPTH stimulates osteoclastic bone resorption, releasing TGFß which recruits these primed progenitors to bone surfaces, a process abolished by osteoclast depletion. Preventing CAR cell maturation via Sp7 deletion abrogates iPTH-induced bone gain, establishing these progenitors as essential mediators of bone anabolism. This coupled mechanism, in which intrinsic transcriptional priming converges with extrinsic niche remodeling, is conserved in human CAR cells from teriparatide-treated postmenopausal women, which show concordant suppression of EBF3 and FOXC1 and elevated TGFß-responsive gene signatures. These findings reveal a general principle by which a systemic hormone orchestrates tissue remodeling through simultaneous reprogramming of progenitor identity and remodeling of the niche microenvironment. - Source: PubMed
Publication date: 2026/05/26
Chan Byron S KDong BingziGeorge MajdWu JuwellAy BirolBrooks Daniel JBouxsein Mary LLeder Benjamin ZPapaioannou GaryfalliaGustafsson KarinScadden David TNagasawa TakashiKronenberg Henry MLin Charles PWein Marc N - Prostate cancer is a highly heterogeneous malignancy, with distinct subtypes displaying unique molecular and metabolic profiles. This study identifies a compensatory shift in α-ketoglutarate (α-KG) metabolism in prostate cancer, where the tumor relies on IDH1 to incorporate citrate into the TCA cycle. IDH1 inhibition, leads to lower α-KG levels. Since α-KG is required for HIF-1α hydroxylation, IDH1 inhibition stabilizes HIF-1α, which subsequently upregulates c-Fos. C-Fos enhances GLUD1 transcription, promoting the conversion of glutamate to α-KG as a compensatory mechanism. Additionally, c-Fos upregulates downstream effectors, including FOXC1 and SOX2, driving neuroendocrine differentiation in prostate cancer. Targeting α-KG-metabolizing enzymes, such as IDH1 or GLUD1, presents promising therapeutic strategies for prostate cancer subtypes by inhibiting tumor proliferation and inducing oxidative stress, thus sensitizing tumors to ferroptosis. Overall, these findings uncover a metabolic adaptation in response to IDH1 inhibition and highlight the pivotal role of c-Fos in mediating this compensatory pathway, offering new insights into potential metabolic targets for prostate cancer treatment and ferroptosis-based therapies. - Source: PubMed
Publication date: 2026/05/31
Ao LiyanChen ZhiqiangZhang JingliangWang QiLuo JinLi ZhuoranJiao QilongNing BobinPeng ShiyuanHu WenhaoJia YuqiCi WeiminWang BaojunDong ZhouhuanZhang XuNiu Shaoxi - Inflammation-induced dysregulation of microRNAs, particularly miR-138-5p, compromises trophoblast cell function and may contribute to pregnancy-related complications. While species have been reported to possess therapeutic properties, the anti-inflammatory effects of Prain (EKP) in trophoblast cells have not been explored. In this study, a 70% ethanolic extract of EKP was fractionated into hexane (HEX), dichloromethane (DCM), ethyl acetate (ETAC), and water (WT) fractions. Each fraction was subjected to phytochemical profiling, antioxidant assessment, and bioactive compound identification by GC-MS and high-performance liquid chromatography (HPLC). Among them, the ETAC fraction (EKP-ETAC) showed the highest antioxidant activity, reflected by the lowest IC values in ABTS and DPPH assays, and contained the greatest levels of phenolic and flavonoid compounds. Nontoxic concentrations were determined by an MTT assay. Pretreatment with EKP-ETAC alleviated lipopolysaccharide (LPS)-induced impairment of proliferation, migration, and invasion in HTR-8/SVneo trophoblast cells, while reducing apoptosis, intracellular ROS generation, and inflammatory cytokine expression. Mechanistic analysis revealed that EKP-ETAC suppressed LPS-induced upregulation of miR-138-5p and restored the expression of FOXC1. The dual luciferase reporter assay confirmed that FOXC1 is a direct target of miR-138-5p, mediating the effects of EKP-ETAC. LC-MS and HPLC analyses identified rosmarinic acid as the predominant bioactive component. These findings suggest that rosmarinic acid-enriched EKP-ETAC exerts protective effects on trophoblast cells by mitigating oxidative stress and inflammation through the miR-138-5p/FOXC1 axis. - Source: PubMed
Publication date: 2026/05/21
Chaiwangyen WittayaKhantamat OrawanOnsa-Ard AmnartKangwan NapapanTipsuwan WachirapornSongkrao AngkanaKatasai ApirakPhngam ApisitNuntaboon PiyawanSangprachum RamitaThippraphan Pilaipornde Sousa Francisco Lázaro Pereira