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)
- 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 - RNAscope™ is a highly sensitive technique for detecting RNA molecules within cells, offering superior specificity and signal amplification compared with traditional in situ hybridization methods. This technique enables the visualization of gene expression patterns at the single-cell level, making it particularly advantageous for studies involving complex tissues or 3D culture systems. In this study, RNAscope™ was used to investigate gene expression within an organ-on-a-chip (OoC), a system that usually encompasses a limited number of cells making the application of standard gene expression analysis techniques, such as qPCR, difficult. In this study, human articular chondrocytes (Chs) isolated from the knee joints of both osteoarthritic patients and heathy donors' cells were encapsulated in a hyaluronic acid (HA)-based hydrogels and injected in a three-channels microfluidic device. RNAscope™ technique was employed directly within the OoC device to study the expression of a long noncoding transcript, FOXCUT, together with FOXC1 and IL-6 in healthy and diseased chondrocytes and there was a correlation between the methylation profile of FOXCUT and osteoarthritis (OA). RNAscope™ enabled the visualization of the spatial localization of target transcripts, including those with low expression levels, such as FOXC1 and FOXCUT. The standard protocol, originally designed for fixed-frozen tissue samples, required optimization to accommodate the unique properties of the OoC environment. Key adaptations included the fixation step using paraformaldehyde, permeabilization with Triton X-100 and an adjusted protease treatment. These modifications were essential to ensure efficient probe penetration and accurate signal detection within the HA 3D matrix. A detailed protocol is herein provided for the detection of RNA within a microfluidic device by using the RNAscope™ technology. - Source: PubMed
Petta DalilaZaninelli FrancescaMoretti Matteo - The evolutionarily conserved Notch signaling pathway is a contact-dependent communication mechanism regulating cell fate, tissue patterning, and cellular metabolism. Beyond canonical NICD-RBPJ transcription, Notch engages in non-canonical crosstalk with networks like Wnt and NF-κB. In tumor angiogenesis, the endothelial Foxc1/2-DLL4-Notch1 axis coordinates tip/stalk cell plasticity, while restricting glycolytic flux via PFKFB3 downregulation to promote vessel maturation. Consequently, pathway inhibition triggers non-productive hypersprouting and vascular collapse, whereas Notch activation strategies offer potential for therapeutic vessel normalization. Crucially, Notch acts as a driving oncogene in B-cell malignancies, promoting survival and chemoresistance. In mantle cell lymphoma (MCL), somatic mutations truncate the C-terminal PEST domain, preventing proteasomal degradation and inducing constitutive NICD hyperactivation-defining an aggressive, microenvironment-sustained clinical subset. Similar NOTCH1/2 aberrations drive clonal progression in marginal zone and MALT lymphomas, and indicate poor prognosis in Hepatitis C Virus-positive diffuse large B-cell lymphoma (DLBCL). Routine genomic screening for Notch alterations provides critical prognostic stratification, laying the basis for personalized, selective therapies in refractory hematological diseases. - Source: PubMed
Publication date: 2026/08/17
Tamma RobertoBenagiano VincenzoRibatti Domenico - To clarify the molecular and clinical characteristics of anterior-segment dysgenesis (ASD)/aniridia and microphthalmia/anophthalmia caused by monogenic variants. - Source: PubMed
Publication date: 2026/07/28
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