FOXC1 antibody
- Known as:
- FOXC1 (anti-)
- Catalog number:
- orb100554
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- FOXC1 antibody
Related genes to: FOXC1 antibody
- 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
Related articles to: FOXC1 antibody
- Acute myeloid leukemia (AML) is a genetically and phenotypically heterogeneous hematological malignancy. Here, to better define this clinically taxing and translationally challenging malignancy, we applied a multiomics approach, consisting of 13 modalities to analyze 173 treatment-naive individuals with AML. By integrating these 'omes', we identified distinct AML subtypes, genotype-phenotype associations, biomarkers and pathobiological mechanisms. Across the spectrum of primitive and committed AML, we found extensive metabolomic and lipidomic reprogramming driven by divergent MYC and mTOR activity. We linked metabolic changes to striking hyperacetylation of mitochondrial proteins in CEBPA-mutant AML. Protein-centric subtyping revealed a distinct NPM1-mutant subset characterized by outlier expression of FOXC1 and HOXB8/9. To nominate therapeutic targets across subtypes, we developed a multiomic machine-learning approach and validated MTA1 as a contributor to panobinostat resistance. Altogether our findings underscore the complex nature of AML and provide a clinically and translationally informed unified view that reveals coalescent phenotypes across multiomic layers. - Source: PubMed
Publication date: 2026/06/12
Chu Shih-Chun AHsiao YiWang ChenweiKyle Jennifer EJain RaghavDeng YameiGritsenko Marina AHenry Leanne ELei Jonathan TDou YongchaoTercan BaharShi ZhiaoGondal Mahnoor NTsai Chia-FengElizarraras John MChu Rosalie KYu FengchaoJoshi Sunil KJing XiaojunPolasky Daniel AWeitz Karl KLi Ginny XiaohePaurus Vanessa LClendinen Chaevien SSchepmoes Athena ALalli Priscila MEder Josie GFlores Javier EStratton Kelly GPino James CPosso CamiloPetyuk Vladislav ASagendorf Tyler JXu YuanweiIbrahim Omar MMoore Ronald JZhao RuiChen JinMonroe Matthew EThiagarajan MathangiHostetter GalenNewton ChelseaAn EunkyungRobles Ana IZhang XuEdwards Nathan JLu YinZhang HuiAbdelhakim HaithamPiehowski Paul DMesri MehdiSmith Richard DKumar-Sinha ChandanTognon Cristina EDunlap JenniferTraer ElieDing LiTyner Jeffrey WChinnaiyan Arul MOmenn Gilbert SRodland Karin DDhanasekaran Saravana MGosline Sara J CNesvizhiskii Alexey IZhang BingLiu TaoCieslik Marcin P - 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