FOXL1 antibody - N-terminal region (ARP32303_T100)
- Known as:
- FOXL1 (anti-) - N-terminal region (ARP32303_T100)
- Catalog number:
- arp32303_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FOXL1 antibody - N-terminal region (ARP32303_T100)
Related genes to: FOXL1 antibody - N-terminal region (ARP32303_T100)
- Gene:
- FOXL1 NIH gene
- Name:
- forkhead box L1
- Previous symbol:
- FKHL11
- Synonyms:
- FREAC7, FKH6
- Chromosome:
- 16q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-06-05
- Date modifiied:
- 2016-10-05
Related products to: FOXL1 antibody - N-terminal region (ARP32303_T100)
Related articles to: FOXL1 antibody - N-terminal region (ARP32303_T100)
- Despite the substantial variability in physical function among older adults, the molecular mechanisms remain poorly characterized, particularly within skeletal muscle. This study aimed to determine the patterns of DNA methylation in skeletal muscle associated with physical function in healthy older adults. We analyzed DNA methylation (EPIC v2 array; 875,554 CpG sites) in skeletal muscle from 92 healthy older adults (median age 74; 62% female). Associations were examined across five phenotypes: Short Physical Performance Battery (SPPB), 6-min walk test (6MWT), handgrip strength, perceived disability (PAT-D), and lifestyle health (modified Life's Essential 8). Linear regression models adjusted for age, sex, race, BMI, and muscle fiber composition. Genomic inflation corrected via the BACON method (FDR < 0.05). Gene set enrichment analysis was performed on suggestive hits (FDR < 0.1). We identified significant differentially methylated probes (DMPs) and regions (DMRs) across all phenotypes: SPPB (70 DMPs, 22 DMRs), 6MWT (16 DMPs, 566 DMRs), handgrip strength (2 DMRs), PAT-D (19 DMPs, 1 DMR), and lifestyle health (2 DMPs). DMRs largely overlapped promoters. Identified genes overlapped known musculoskeletal and neurological GWAS hits, including RUNX2 and FOXL1 (bone mineral density), IGFBP3 (muscle mass), and NEK1 and SHANK1 (neurological function). Enrichment analysis revealed that 6MWT-associated genes relate to nervous and skeletal system development, while handgrip-associated genes involve cytoskeletal dynamics and protein assembly. Epigenetic variation in aging skeletal muscle is associated with physical function. The enrichment of pathways related to nervous and musculoskeletal development suggests specific epigenetic mechanisms underlying functional decline, offering potential targets for intervention in older adults. - Source: PubMed
Publication date: 2026/08/08
Wen XiaoxiaoChen MingjingMiao GuanhongWu ChristopherPicca AnnaTamargo Javier ALou XiangyangWu KevinAnton StephenLeeuwenburgh ChristiaanZhao Jinying - Telocytes are stromal cells defined by extremely long, moniliform prolongations termed telopodes and have been described in most mammalian organs since their formal designation in 2010. During the past two decades, the field has expanded from ultrastructural organ-mapping to hypotheses concerning stem-cell niche regulation, extracellular-vesicle-mediated communication, fibrosis, inflammation, and cancer-associated stromal remodelling. This expansion, however, has also generated methodological heterogeneity, with frequent reliance on non-specific markers such as CD34, PDGFRα, vimentin, and c-kit, often without ultrastructural validation or functional perturbation. In this critical review, we reassess the evidential status of major claims in telocyte biology, distinguishing robustly demonstrated mechanisms from plausible but incompletely proven hypotheses. The strongest functional evidence remains the conditional ablation of Wnt secretion in intestinal Foxl1-/Gli1-expressing subepithelial telocytes, which demonstrates their necessity for stem-cell niche maintenance. By contrast, most evidence from cardiac, dermal, reproductive, and fibrotic tissues remains supplementation-based or correlative. We propose a unified Stromal Network Organiser framework, in which telocytes are interpreted as tissue-specific stromal network cells whose dysfunction may involve not only numerical loss, but also telopode fragmentation, contact uncoupling, paracrine alteration, stromal replacement, and failed niche signalling. To improve methodological clarity, we introduce a two-dimensional evaluation matrix that separates identification confidence from functional confidence. We argue that the next decade of telocyte research should prioritise loss-of-function experiments outside the intestine, independent replication of foundational single-laboratory concepts, and high-resolution multi-organ correlative ultrastructural atlases. - Source: PubMed
Publication date: 2026/07/11
Pavelescu Luciana AlexandraCrețoiu Sanda Maria - Intestinal epithelial cells rely on a complex array of stromal signals to determine their fate and function along the crypt-villus axis, but the precise cellular sources and combinations of signals at each position remain poorly defined. - Source: PubMed
Publication date: 2026/07/16
Gharbi AmalCorem NoaElgavish SharonaPlachkes InbarJamous AbrarCanella MarcoShmuel MoriyaHorowitz HadarTan JianmeiChen HongqianSu BingAbu-Gazala MahmudShussman NoamShoshkes-Carmel Michal - The human small intestine depends on villi to generate the large absorptive surface area required for nutrient uptake and barrier integrity. Existing human in vitro models fail to reproduce early villus morphogenesis, as they lack developmental signaling and epithelial-mesenchymal interactions that drive villus initiation. Such models are crucial for understanding the mechanisms of human villus formation to study intestinal development and disease. This study aimed to establish a human organotypic intestine model that recapitulates early villus development and to compare its features with human embryos. Primary organoid-derived epithelial cells containing intestinal stem and progenitor populations, and Caco-2/HT29 cocultures (as reference) were both cultured on a hydrogel containing primary small-intestinal stromal cells in a Transwell system. Models were assessed by histology, electron microscopy, transepithelial electrical resistance (TEER), permeability assays, gene expression analysis, growth factor secretion, and comparison with human embryonic duodenum (Carnegie stages 20-23). Both models formed polarized epithelial monolayers with sparse microvilli compared with mature intestine. Strikingly, only the organoid-derived model generated stromal cell and extracellular matrix (ECM)-filled epithelial protrusions with localized laminin deposition. This model activated key developmental pathways (SHH, PDGF-AA, BMP4, and WNT5A), upregulated villus-associated transcription factors (FOXF1, FOXF2, and FOXL1), and expressed laminin isoforms linked to villus initiation. The morphology and height of the protrusions (approx. 28 µm) closely resembled early villi in Carnegie stage 21 embryos. - Source: PubMed
Publication date: 2026/07/15
Asal MelisPaauw Nanne JThon MariaWaaijman TacoMorrison Andrew IMulder Puck Pde Bakker Bernadette SBontkes Hetty Jvan Vliet Sandra JMebius Reina EGibbs Susan - Recurrent spontaneous abortion (RSA) is a major pregnancy complication with largely unknown causes. Carbohydrate metabolism (CM) disorders can affect the progression of endothelial cell senescence (ES), thereby leading to placental dysfunction. However, research on the interplay between CM and ES in RSA is limited. This study aims to identify key genes at the intersection of CM- and ES-related pathways in RSA via various bioinformatics methods. - Source: PubMed
Publication date: 2026/06/24
Chen LinShao YuPan XianshunLai Ting