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)
- Sorafenib refractoriness severely compromises therapeutic efficacy in hepatocellular carcinoma (HCC). This study identifies ferritin heavy chain 1 pseudogene 7 (FTH1P7) as a critical driver and propagator of sorafenib resistance. FTH1P7 was significantly upregulated in HCC cells resistant to sorafenib. Mechanistically, the self-sustaining FTH1P7/microRNA-182-5p/FOXC1 positive feedback loop maintained high FTH1P7 expression levels in resistant cells. Elevated FTH1P7 functioned as a competing endogenous RNA to the mRNA of its parental gene, ferritin heavy chain 1 (FTH1). Increased FTH1 levels enhanced Fe oxidation, thereby inhibiting ferroptosis-a key anticancer mechanism of sorafenib-thereby conferring resistance. Furthermore, exosomes derived from resistant cells transferred FTH1P7 to sorafenib-sensitive cells, thereby horizontally propagating resistance. To counter sorafenib resistance, we developed a nanoliposome co-delivering sorafenib and FTH1P7-targeting siRNA (SR-siFTH1P7-LIP). This nanomedicine synergistically and effectively silenced FTH1P7 expression and reversed resistance. These results elucidate novel mechanisms of sorafenib resistance, involving FTH1P7-mediated induction and exosomal propagation of ferroptotic resistance, and propose a promising nanomedicine-based strategy to combat sorafenib refractoriness in HCC. - Source: PubMed
Publication date: 2026/08/03
Cao SisiXiong ChuanweiWu JiayuanQin MeiZou QingrongDeng JinlanPeng SiqiHe LinhongHuang ZijunYang JieQin MeichunChen WenkaiZhang XiaopingLiu LinDong Min - Cerebral small vessel diseases (CSVDs) are a group of disorders affecting the small arteries, veins, and capillaries supplying the white matter and deep grey matter structures. They are the most common form of cerebrovascular disease, accounting for approximately half of vascular dementia cases and 20% of stroke incidence. Whilst genetic testing is a routine diagnostic tool for monogenic CSVDs, less than 20% of patients have a causal variant in known CSVD genes. We performed whole exome sequencing on 117 patients suspected of monogenic CSVD who previously tested negative for pathogenic variants in seven well-characterised CSVD genes (NOTCH3, HTRA1, COL4A1, COL4A2, TREX1, GLA, and FOXC1). Targeted analysis was conducted on known and associated CSVD genes, as well as candidate genes which cause conditions with overlapping symptomology to CSVD. Burden analysis focussing on rare, functional variants was used to identify novel associations when compared against a cohort of 1035 non-neurological controls. We identified 18 suspected disease-causing variants across nine CSVD-associated genes and a significant burden of both rare and rare, likely disease-causing heterozygous variants in ABCC6. Two genes from stroke and neurodegenerative disease gene panels also possessed a significant burden of rare, likely disease-causing variants, MYH11 (adjusted P = 1 × 10) and NOTCH1 (adjusted P = 1 × 10). We further identified novel associations for seven genes (COL7A1, HMCN1, LAMA1, MMP9, TENM4, TNC, TTN) with monogenic CSVD in this cohort. Our findings implicate several genes as potentially causal of monogenic CSVD, highlighting the need for more extensive genetic screening in suspected CSVD cases, and functional characterisation of implicated variants to determine their mechanistic role in CSVD pathogenesis. - Source: PubMed
Publication date: 2026/07/21
Guyler Solomon KAlfayyadh Mohammed MMaksemous NevenLea Rodney ASmith Robert ASutherland Heidi GGriffiths Lyn R - The instability of atherosclerotic plaques, particularly intraplaque hemorrhage (IPH), drives life-threatening cardiovascular events, a process in which vascular smooth muscle cell (VSMC)-derived foam cells play a significant role. We aim to identify key biomarkers associated with VSMC-derived foam cells and IPH by analyzing data from human IPH datasets and VSMC-derived foam cell datasets (GSE163154, GSE68021, GSE28829, and GSE43292). Weighted gene co-expression network analysis (WGCNA), differential expression analysis, and machine learning algorithms (LASSO and SVM-RFE) were employed to identify hub genes. The identified genes were validated in independent datasets and in experimental models, including oxidized low-density lipoprotein-stimulated VSMCs and atherosclerotic aortic tissues of high-fat diet-fed ApoE/ mice. Transcription factor (TF) prediction and dual-luciferase reporter assays were performed to explore upstream regulatory mechanisms. We identified CD68 and CYBA as key hub genes significantly upregulated in both VSMC-derived foam cells and unstable atherosclerotic plaques, with high diagnostic accuracy (AUC > 0.9) by ROC analysis. Experimental validation confirmed their upregulated expression. FOXC1 was identified as a common upstream transcription factor regulating both CD68 and CYBA. FOXC1 protein levels were elevated in VSMC-derived foam cells, and dual-luciferase assays confirmed its direct activation of CD68 and CYBA promoters. FOXC1 overexpression promoted CD68 and CYBA expression and enhanced lipid accumulation in VSMCs, while FOXC1 knockdown exerted opposite effects. Immune infiltration analysis revealed significant correlations between these hub genes and immune cell populations in unstable plaques. This study identifies FOXC1 as a key TF regulating CD68 and CYBA expression, thereby promoting VSMC-derived foam cell formation and plaque instability. - Source: PubMed
Publication date: 2026/07/20
Qian Ling-LinLi Xue-LingWang Li-HongYang WeiJiang Yu - Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive degeneration of midbrain substantia nigra dopaminergic neurons, resulting in striatal dopamine depletion and motor dysfunction. While this pathological cascade is well-established, its underlying mechanisms remain elusive. - Source: PubMed
Publication date: 2026/07/14
Qin BinqingFu ZichuZou XuanxuanChai SenmaoWeng JingjingWang PuqingSun XiaodongSang Ming - Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer (BC) with limited treatment options. Paclitaxel (PTX) is commonly used, but its effectiveness is hampered by resistance and metastasis. The c-Met receptor, which is often upregulated in TNBC, promotes tumor progression via the HGF/c-Met axis and downstream PI3K/AKT and MAPK pathways. This study explored whether Capmatinib (CAP), a selective c-Met inhibitor, can enhance PTX efficacy in TNBC. - Source: PubMed
Publication date: 2026/07/13
Sezavar Ahmad HabibianFakhari FatemehJafarzadeh EmadMontazeri VahidehShadborestan AmirAbdollahi MohammadSabzevari OmidKebriaeizadeh AbbasHosseini RuhollahAliebrahimi ShimaOstad Seyed Nasser