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 highly heterogeneous hematologic malignancy in which relapse and acquired chemoresistance remain major causes of treatment failure. This article presents a bioinformatic protocol for transcriptomic analysis of bone marrow aspirates. The primary goal of the protocol is to provide a standardized workflow to identify molecular signatures associated with disease progression and therapy resistance in relapsed AML. The pipeline details the computational procedures for comparing unpaired bone marrow samples, demonstrated using sequencing data from five newly diagnosed cases and four relapsed cases. This method outlines the essential steps for processing RNA sequencing data, performing differential gene expression analysis, and conducting downstream functional evaluations. Applying this workflow identified 2,025 differentially expressed genes (DEGs), including FOXC1, HOXA11, HOXA11-AS, and AXL, as candidate transcripts associated with relapse in this representative dataset. Functional and network analyses further prioritized gene sets and interaction hubs related to small GTPase signaling, inflammatory signaling, extracellular matrix interactions, and RNA biosynthetic processes. Overall, this methodology provides a reproducible computational pipeline for mapping transcriptomic signatures associated with relapsed AML and for generating hypotheses that require subsequent experimental validation. - Source: PubMed
Publication date: 2026/08/04
Hu JingGuo ZhiWan BolinHe ChengmingZou Min - Metronomic chemotherapy (MCT), understood as continuous, low-dose cytotoxic administration without prolonged drug-free intervals, has become an established strategy in several solid tumors, acting primarily through antiangiogenic, immunomodulatory, and direct cytostatic mechanisms rather than replication-dependent cytotoxicity. Despite an expanding evidence base, including positive randomized trials, validated predictive biomarkers of response remain unavailable. - Source: PubMed
Publication date: 2026/08/03
Wysocki Piotr JanKwinta ŁukaszWysocka Ewa - Triple-negative breast cancer (TNBC) is a biologically heterogeneous, aggressive disease where immunohistochemistry (IHC)-based algorithms, defining luminal androgen receptor (LAR), immunomodulatory (IM), basal-like immunosuppressed (BLIS), mesenchymal (MES), and unclassifiable (UC) subtypes, offer a pragmatic alternative to transcriptomics. This study evaluated clinical trajectories and survival outcomes associated with IHC-based molecular subtypes and stromal tumor-infiltrating lymphocytes (sTILs) across distinct subgroups. - Source: PubMed
Publication date: 2026/08/12
Hernandez-Hernandez Jesus EdgardoMohar AlejandroLara-Torres César OctavioVazquez-Juarez DanielaPalacios TamaraPeña-Torres LourdesMoncada-Claudio GuadalupeVelazquez-Martinez AreliCabrera-Galeana PaulaGómez-Macías Gabriela SofíaPorras-Reyes Fany IrisPérez-Sánchez Víctor ManuelAranda-Gutierrez AlejandroVillarreal-Garza Cynthia - 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