Ask about this productRelated genes to: CD49e antibody
- Gene:
- ITGA5 NIH gene
- Name:
- integrin subunit alpha 5
- Previous symbol:
- FNRA
- Synonyms:
- CD49e
- Chromosome:
- 12q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1988-07-19
- Date modifiied:
- 2016-01-15
Related products to: CD49e antibody
Related articles to: CD49e antibody
- Ochratoxin A (OTA), a prevalent food contaminant, is closely linked to the development of various cancers, including clear cell renal cell carcinoma (ccRCC). However, the potential mechanisms remain to be explored. In this study, we employed network toxicology, machine learning, and molecular docking techniques to systematically investigate the potential molecular mechanisms underlying OTA-associated ccRCC. We normalized transcriptional data from two Gene Expression Omnibus (GEO) datasets and analyzed it using differential expression analysis and weighted gene co-expression network analysis (WGCNA), identifying 3224 ccRCC-associated target genes. These were intersected with 232 predicted OTA target genes, yielding a total of 56 overlapping targets. The results of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses indicated that these targets were primarily enriched in critical biological processes, including extracellular matrix remodeling, immune microenvironment regulation, signaling pathway transduction, cellular metabolism, and protein homeostasis. Machine learning analysis identified "glmBoost + RF" (a sequential combination of feature selection and classifier) as the optimal model, from which nine key genes were extracted. SHapley Additive exPlanations (SHAP) analysis revealed five core genes (, , , , ), with and serving as the principal driver genes of the model. Validation of the model's diagnostic efficacy and single-cell transcriptome analysis indicated that the core genes exhibited significant differential expression patterns, cell-type-specific expression characteristics, and high independent diagnostic efficacy. Molecular docking analyses predicted stable interactions between OTA and the core target proteins. These findings suggest potential molecular links between OTA exposure and ccRCC, providing a foundation for hypothesis generation and future experimental validation. - Source: PubMed
Publication date: 2026/03/25
Huang ChenjieWei LuluYuan WenqiLu YaohongYan ZiyouZhang Gedi - 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 - Pulmonary fibrosis (PF) arises from persistent fibroblast activation and inflammation. Although microRNAs (miRNAs) are promising antifibrotic agents, the contribution of adipose-derived circulating miRNAs to PF remains unclear. Here, we identify brown adipose tissue (BAT) as a major source of exosomal miR-378a-3p that counteracts bleomycin (BLM)-induced PF. In fibrotic mice, BAT activity and circulating exosomal miR-378a-3p were reduced. Activating BAT by cold exposure or β3-adrenergic stimulation increased circulating and pulmonary miR-378a-3p and attenuated collagen deposition and inflammatory infiltration. Adipocyte-specific deletion of miR-378a-3p exacerbated lung inflammation and fibrosis, whereas lung-targeted overexpression of miR-378a-3p or intravenous delivery of BAT-derived exosomes enriched for miR-378a-3p ameliorated disease. Inhibition of exosome release from BAT lowered circulating miR-378a-3p and blunted the anti-fibrotic benefits of BAT activation, supporting a BAT-to-lung transfer mechanism. Mechanistically, miR-378a-3p targets Itga5 to suppress FAK-PI3K-AKT signaling and limiting fibroblast activation, while simultaneously suppressing macrophage inflammatory responses by targeting Fstl1 and suppressing NF-κB activation. Collectively, these findings identify miR-378a-3p as a BAT-derived signaling molecule with dual anti-inflammatory and anti-fibrotic effects in pulmonary fibrosis, expanding the pathophysiological scope of BAT-mediated inter-organ communication to lung disease. - Source: PubMed
Publication date: 2026/03/28
He RuiPeng XueminPan RupingKang QianqianLiu ShulinYang MinWang ZhihanDeng HongyanLi DanpeiXie YuyuWang WensheZhu ZengzheLiu JiadaiGe JingLiu YulianGao RonghuiYang YanChen Yong - - Source: PubMed
Publication date: 2026/03/10
Zhang WeilinHuang ShengbangLiu KuizeFeng DaoLiang JinguoLi ZhencongZhou BoyuanDai ZhiwenWang ZhongweiWei Jinsong - Among breast cancer subtypes, triple-negative breast cancer (TNBC) stands out for its aggressiveness and high frequency of brain metastases. However, the mechanisms driving BrM remain poorly understood. - Source: PubMed
Publication date: 2026/03/09
Zhou QiyiZhu ZhiminZhao YuxinJing DiZhang Liyuan