Ask about this productRelated genes to: CD49d antibody
- Gene:
- ITGA4 NIH gene
- Name:
- integrin subunit alpha 4
- Previous symbol:
- CD49D
- Synonyms:
- CD49d
- Chromosome:
- 2q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-06
- Date modifiied:
- 2016-10-05
Related products to: CD49d antibody
Related articles to: CD49d antibody
- Epigenetic modifications, especially DNA methylation, play an increasingly important role in oral cancer. However, their specific contributions to the progression of oral squamous cell carcinoma (OSCC) remain unclear. The present study used the Shiny Methylation Analysis Resource Tool (SMART) database (https://smart.embl.de/smart/change_mode.cgi) to identify methylation‑driven genes associated with OSCC. Among the identified candidates, integrin subunit α4 (ITGA4) exhibited significantly elevated methylation levels in head and neck cancers. A methylation‑specific PCR assay showed that ITGA4 is highly methylated in OSCC cells compared with normal immortalized human normal oral keratinocyte (iNOK) cells. Additionally, the mRNA expression levels of ITGA4 were significantly lower in OSCC cell lines compared with normal iNOK cells. ITGA4 overexpression markedly inhibited the cell proliferation, migratory ability and capacity of colony formation and induced apoptosis in FaDu and YD‑15 cells. In proteomic analysis, ITGA4 suppressed the expression of Sorting Nexin 5 (SNX5), a protein linked to cancer progression. siRNA‑mediated knockdown of SNX5 importantly inhibited cell proliferation, migration, and colony formation in FaDu and YD‑15 cells. Moreover, in a chick chorioallantoic membrane xenograft model, overexpression of ITGA4 or small interfering SNX5 significantly inhibited OSCC tumor growth and angiogenesis . Collectively, these findings demonstrated that ITGA4 acts as a tumor suppressor in OSCC by downregulating SNX5 and suggested that ITGA4 may serve as a valuable prognostic biomarker and potential therapeutic target for OSCC. - Source: PubMed
Publication date: 2026/04/24
Tien Nguyen Ngoc ThuyChoe Han-CheolAhn Sang-Gun - Severe burn injuries represent a major global healthcare burden, with high costs and prolonged hospitalizations. Current treatments, including autologous skin grafting, are limited by donor availability, while allografts carry risks of immune rejection. Advanced Therapy Medicinal Products (ATMPs) offer a promising alternative for skin substitution. We evaluated the efficacy of ARTSkin, an alginate-modified bacterial nanocellulose-based ATMP, in a murine model of third-degree burns. ARTSkin was manufactured under good manufacturing practice (GMP) conditions in two formulations: an acellular scaffold and a cellular construct containing human dermal fibroblasts. The acellular formulation was first assessed in vitro for cytotoxicity and wound-healing capacity using a scratch assay. In vivo, acellular and cellular ARTSkin were evaluated in immunocompetent and immunosuppressed mice, respectively. Acellular ARTSkin was non-cytotoxic and enhanced fibroblast migration and proliferation in vitro. Both formulations significantly improved wound healing in vivo, with accelerated closure and reduced bleeding, hyperemia, edema, and crust formation. Transcriptomic analysis showed that cellular ARTSkin modulated genes involved in the proliferative phase of healing by preventing burn-induced dysregulation of Rac1, Vegfa, and Itga4, and downregulating the profibrotic gene Ctgf. These findings support ARTSkin as a promising skin substitute for burn therapy. - Source: PubMed
Publication date: 2026/04/21
Machado Godoi ManuellaPeruzzi Caroline PortelaHoepers Joao Vitor Alvesda Silva Ana Meriando Nascimento Henrique Sant'Ana KoeppMateus Felipe NascimentoGonçalves Ana CarolineColla GuilhermeKoepp JaniceFerreira Juliano - Acute myeloid leukemia (AML) is a hematologic malignancy with high relapse rates and limited treatment options due to extensive intra-tumor heterogeneity across patients. To characterize this heterogeneity, we profiled matched bone marrow mononuclear cell (BMMC) samples from 26 patients with adult AML at diagnosis and relapse using the cellular indexing of transcriptome and epitope sequencing (CITE-seq) and quantitative flow cytometry. These data together represent a comprehensive multimodal and longitudinal single-cell resource that reveals the transcriptomic and immunophenotypic landscape of AML. Data integration of CITE-seq and flow cytometry surface antigen readouts enabled systematic quantitation of surface antigen co-expression across individual leukemic cells, providing a granular framework for the design of immunotherapeutic strategies to target heterogeneous AML. With this resource, we identified CD33, CLL-1, LAIR1, ITGA4, DEC-205, and CD244 as antigens that induced cytotoxicity in AML cell lines when co-targeted by antibody drug conjugates (ADCs) or chimeric antigen receptor T (CAR-T) cells, demonstrating the exploitation of AML heterogeneity for immunotherapeutic innovation. - Source: PubMed
Publication date: 2026/03/11
Ung MatthewEtchin JuliaHalfond AmandaDiFazio JuliaKeschner YoninaPyclik AlyssaCampbell AnneWang RuijiaSilva MarianaGjeci BrikenaMontalbano AntoninoWilliams ReidMundelboim GuyArruda AndreaMinden MarkScherer JulianChakraborty TirthaGe Huanying GaryLydeard John R - This study develops a computational framework integrating bioinformatics, machine learning, and ΔG clustering to prioritize polycyclic aromatic hydrocarbons (PAHs) for Alzheimer's disease (AD)-associated neurotoxicity. PAH targets were predicted from ChEMBL/STITCH databases; AD-related differentially expressed genes (DEGs) were identified via WGCNA and differential expression analysis of GEO datasets. Protein-protein interaction (PPI) networks, GO/KEGG enrichment, and XGBoost feature selection identified PARP1, PTPN1, and ITGA4 as candidate core PAH targets enriched in neuroinflammation, microglial activation, lipid metabolism, and atherosclerosis pathways. Molecular docking produced ΔG heatmaps for clustering 16 PAHs into eight toxicity-similarity categories. Category-average ΔG values correlated linearly with literature LD/BMDL data (ρ = 1, = 0.0417), yielding an empirical relationship BMDL = 1.723 × ΔG + 22.602. Zebrafish motility assays provided preliminary support (Spearman ρ = -1.0, = 0.167; = 3). This pipeline provides initial insights into PAH mechanisms and potential therapeutic targets, pending experimental validation. - Source: PubMed
Publication date: 2026/03/11
Chen ChaoHe YuxiNi YingSong DongyanChu MaopingZhang Wensheng - Thoracic aortic aneurysm (TAA) is a life-threatening condition characterized by aortic dilation, inflammation, and extracellular matrix degradation. Despite advances in surgical management, effective pharmacological therapies are still lacking, largely due to an incomplete understanding of the cellular mechanisms driving disease progression. Although recent single-cell RNA sequencing (scRNA-seq) studies have revealed diverse cell types in TAA, the intercellular communication driving pathological remodeling is still poorly defined. Here, we performed integrated scRNA-seq analysis of human TAA (n = 8) and healthy aorta (n = 8) to construct a comprehensive cellular landscape. We identified a disease-associated crosstalk between myeloid cells and fibroblasts, mediated by SPP1 and MK signaling. These two cell subsets were enriched in TAA and co-activated TNF-α signaling via NF-κB and epithelial mesenchymal transition (EMT) pathways, thereby promoting inflammation and ECM remodeling. Cell-cell communication analysis further uncovered upregulated interactions involving SPP1-integrin (e.g., ITGAV/ITGA8/ITGA5+ITGB1) and MDK receptors (SDC4/SDC2/NCL/LRP1/ITGA4/ITGA6+ITGB1) in TAA. These computational findings were further supported by multiplex immunofluorescence and spatial transcriptomics analyses. By integrating key genes and signaling pathways, we identified hub genes and their associated transcription factors, whose regulatory activity was further supported by transcription factor regulon analysis. Our findings highlight the crucial role of myeloid-fibroblast interactions in driving TAA pathogenesis and identify potential therapeutic targets. - Source: PubMed
Publication date: 2026/03/04
Ju YingjiaoYao JingyiZhang SongWu JiangxuXiang JiongaoMin LiLiu Mingyuan