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)
Ask about this productRelated 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)
- Triple-negative breast cancer (TNBC) comprises biologically distinct subtypes, including luminal androgen receptor (LAR) tumors, but routine immunohistochemical markers incompletely capture lineage-associated differentiation states. We investigated TFAP2B, an AP-2 family transcription factor linked to epithelial differentiation, and FOXC1, a basal-like-associated transcription factor, as complementary markers of luminal and basal differentiation in TNBC. In a tissue microarray of 105 TNBCs, tumors were stratified as TFAP2B-dominant, FOXC1-dominant, or double-negative according to relative marker predominance and characterized using lineage, proliferation, molecular, immune, and chemotherapy-response parameters. TFAP2B-dominant tumors were associated with a coherent luminal phenotype, including apocrine/lobular enrichment, strong MUCL1 and AR expression, high CK18, low SOX10, reduced proliferation, frequent wild-type p53 patterns and retained RB1 expression, and low PD-L1 expression. FOXC1-dominant tumors showed contrasting basal-like features. These associations were independently supported at the transcriptional and genomic levels in the METABRIC TNBC cohort. FOXC1-dominant tumors also showed more frequent chemotherapy-induced downstaging than TFAP2B-dominant tumors. Together, we identify TFAP2B as a marker associated with luminal differentiation in TNBC and support combined TFAP2B/FOXC1 assessment as a practical framework for identifying clinically relevant TNBC differentiation states. - Source: PubMed
Publication date: 2026/09/11
Klaus Franz-LeonardKitzke IsabellaKlein EvelynKiechle MarionMogler CarolinMuckenhuber Alexander - Axenfeld-Rieger syndrome (ARS) is a rare genetic disorder characterised by a broad phenotypic spectrum and variable expressivity with characteristic ocular anterior segment dysgenesis, glaucoma and systemic manifestations. ARS is primarily associated with pathogenic variants in and , which both exhibit autosomal dominant inheritance with overlapping ocular findings but distinct systemic manifestations.Numerous different variants in and have previously been described. Here we present a patient with heterozygosity for a previously unreported pathogenic variant in and a phenotype with significant ocular anterior segment dysgenesis, thereby contributing relevant clinical information about the genetic and phenotypic spectrum of ARS, reproductive considerations and importance of genetic counselling. - Source: PubMed
Publication date: 2026/09/11
Nøhr Thomas KromannLarsen Dorte AncherStougaard MagnusTelinius NiklasEngholm MortenGregersen Pernille A - The pathogenesis of diabetic kidney disease (DKD) is complex and closely related to ferroptosis and immune dysregulation, but the relevance is unclear. The present study investigates the potential mechanisms of ferroptosis-related genes (FRGs) in DKD and their relationship with the immune-inflammatory response. It searches for new diagnostic biomarkers to help diagnose and treat DKD. Four Gene Expression Omnibus (GEO) datasets, GSE30528, GSE30529 and GSE30122 as the test set, and GSE96804 for validation, were analyzed. FRGs were obtained from GeneCards, and 47 ferroptosis-related differentially expressed genes (FRDEGs) were identified by intersecting with DKD-related differentially expressed genes. Functional enrichment analyses, including Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, Gene Set Enrichment Analysis and Gene Set Variation Analysis, revealed that these FRDEGs are primarily associated with ferroptosis, hypoxia response and immune inflammation. Subsequently, the weighted gene co-expression network analysis (WGCNA) was employed to expand the ferroptosis-related gene network, and intersection of the 47 FRDEGs with key WGCNA module genes yielded 10 key genes. Based on the 10 key genes, the least absolute shrinkage and selection operator and support vector machine algorithms identified three hub genes [chemokine ligand 5 (CCL5), forkhead box C1 (FOXC1) and lactotransferrin (LTF)] for DKD diagnosis. Receiver operating characteristic curves confirmed their diagnostic value, with FOXC1 and LTF validated in the independent dataset. Immune infiltration analysis via CIBERSORT revealed eight immune cell types with significantly different infiltration levels between the DKD and control group in the integrated GEO datasets. Notably, both LTF and CCL5 showed a significant positive correlation with gamma delta T cells (γδT). Quantitative PCR results confirmed differential expression of the three hub genes in the DKD group, with elevated expression observed in DKD mice following intervention with rosiglitazone and hyperoside. - Source: PubMed
Publication date: 2026/08/28
Tan YingLiu ZihuiSong SiyuanZhu LinglingShe YunZhou XiqiaoYu JiangyiYan Qianhua - SEI1 is overexpressed in multiple myeloma and correlates with poor prognosis. In this study, we identify SEI1 as a crucial driver of myeloma pathogenesis through a previously unrecognized mechanism: transcriptional inactivation of the tumor suppressor p53. Mechanistically, SEI1 forms a transcriptional complex with histone deacetylase 1 (HDAC1) and forkhead box C1 (FOXC1), which binds to the promoter, decreases histone H3 lysine 27 acetylation (H3K27ac), and suppresses transcription, thereby promoting myeloma cell proliferation. SEI1 enhances the stability of the HDAC1-FOXC1 interaction, further amplifying p53 repression. High-throughput virtual screening has identified tiludronate disodium as a potent inhibitor of FOXC1. Tiludronate disodium disrupts the HDAC1-FOXC1 interaction, restores H3K27ac enrichment and p53 expression, and suppresses myeloma growth both and , including a reduction of osteolytic lesions. These findings elucidate the SEI1/HDAC1/FOXC1/p53 axis as a critical driver of myeloma progression and identify tiludronate disodium as a potential therapeutic agent. - Source: PubMed
Publication date: 2026/08/24
Chen RuiLiu RuiFang ZhihongYang DaoyanLi ZouLi YuanLi YuanLiu ShurongLiu QiChao YanqiWang ChongLiu Huan - Pulmonary arterial hypertension (PAH) is a progressive vascular disorder characterized by pulmonary vascular remodeling and endothelial dysfunction. Although several molecular regulators have been implicated in PAH pathogenesis, the key transcriptional networks governing these processes remain incompletely understood. This study aimed to investigate the role of the transcription factor forkhead box C1 (FOXC1) in PAH development and evaluate its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/09/04
Li SijiaYang MingyuChen HongyuChen ShifanLiao JielinLiu JiayanLi JuRan YajuanYu Xiufeng