Thy1 binding protein EMSA Kit
- Known as:
- Thy1 binding protein EMSA Kit
- Catalog number:
- AY1414
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- Thy1 binding protein EMSA Kit
Related genes to: Thy1 binding protein EMSA Kit
- Gene:
- THY1 NIH gene
- Name:
- Thy-1 cell surface antigen
- Previous symbol:
- -
- Synonyms:
- CD90
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2015-07-22
Related products to: Thy1 binding protein EMSA Kit
Related articles to: Thy1 binding protein EMSA Kit
- Pulmonary fibrosis (PF) is a progressive and fatal lung disorder driven by abnormal fibroblast activation and excessive extracellular matrix (ECM) deposition, leading to structural and functional decline. Existing therapies can slow progression but fail to interrupt fibrotic remodeling. Here, we engineered HUCMSC-Lipo, an inhalable biomimetic formulation fusing human umbilical cord mesenchymal stem cell (HUCMSC) membranes with artificial phospholipids, with formulation parameters systematically optimized using a Bayesian optimization (BO) framework to ensure structural stability and nebulization compatibility. HUCMSC-Lipo maintained membrane functionality and structural integrity for effective nebulized delivery. We successfully established a non-human primate (NHP) PF model and innovatively developed a multidimensional evaluation framework. Utilizing a range of methods, including but not limited to positron emission tomography/computed tomography (PET/CT) molecular imaging with radiolabeled fibroblast activation protein (FAP) inhibitors, we confirmed that HUCMSC-Lipo suppressed fibrotic progression and restored pulmonary function by targeting the regulation of fibroblast activation. Mechanistically, THY-1 enrichment in HUCMSC-Lipo bound integrin receptors to block the FAK/PI3K signaling cascade and restore fibroblast mechanosensitivity, fundamentally turning off the pathological activation "switch" in fibroblasts. Our work presents an inhalable biomimetic formulation that combines therapeutic efficacy with synthetic accessibility, offering a mechanism-targeted approach to PF treatment with strong clinical translatability. - Source: PubMed
Publication date: 2026/08/04
Zhao FangyuSun YigeWang HaoranHou DayongZhang RuiXia WenjingZhang YongchenLi LuyaoZhao XueqiWang KaiqiPan WenwenWang JiannanWang KaiYang LiliChen WeiLi XinNong ChunyangLu HuiyingZhang YiZhang ZhaoyangWu LinaHan ZhaoguoTang Ben-ZhongSun Xilin - Osteoarthritis (OA) is the most prevalent degenerative joint disease worldwide and imposes a substantial public health burden due to the lack of effective disease-modifying drugs. Exosome-related genes participate in exosome biogenesis, cargo sorting, and secretion, serving as critical regulatory elements in exosome-mediated intercellular communication. However, their systematic characterization in OA and their potential as diagnostic or therapeutic targets remain largely unexplored. We obtained OA and normal control samples from the GEO database. Using exosome-related gene signatures as a filtering strategy, we integrated differential expression analysis, protein-protein interaction network assessment, and machine learning algorithms to screen for key diagnostic genes, and constructed and externally validated diagnostic models and nomograms. Enrichment analysis and immune infiltration assessment were performed to explore biological functions and immune microenvironment features. Cellular experiments were conducted to validate the effects of the prioritized gene THY1 on chondrocyte apoptosis, senescence, mitochondrial function, and cell viability. We successfully identified THY1, FAP, and TIMP4 as independent diagnostic markers for OA and constructed a diagnostic model and nomogram with high applicability, whose reliability was validated in an external validation cohort. Enrichment and immune infiltration analyses preliminarily identified two OA subtypes with distinct immune infiltration profiles. Cellular experiments confirmed that THY1 overexpression promoted chondrocyte senescence and apoptosis under OA-like inflammatory conditions, while impairing mitochondrial function and cell viability. Through bioinformatic screening and in vitro experimental validation, this study reveals the pro-apoptotic and pro-senescent regulatory effects of THY1 on chondrocytes under inflammatory conditions, and establishes a diagnostic model and subtyping framework for OA based on three genes, offering new perspectives for stratified diagnosis and future translational research in OA. - Source: PubMed
Publication date: 2026/08/25
Huang LiangkunWen YaXu HanzheZhang ZePei ZijieZhao PiqianSun Fengpo - The role of histidine metabolism in heart failure (HF), particularly its heterogeneous regulation across cardiac cell types, remains unclear. This study aims to define its mechanistic basis and identify key regulatory genes. - Source: PubMed
Publication date: 2026/08/10
Xiao SonglinMo ChunleiLiu QixingXu Li - Heterogeneity in cancer-associated fibroblast (CAF) infiltration within the tumor microenvironment is closely associated with gastric cancer progression and immune evasion; however, precise CAF-related diagnostic markers and actionable therapeutic targets remain scarce. - Source: PubMed
Publication date: 2026/08/21
Hou SihuiSang MengzhuWang YanQue HaoshengLiu YiZhang Manman - Cancer-associated fibroblasts (CAFs) are key components of the tumor microenvironment and play important roles in cancer progression and treatment resistance. Despite recognized heterogeneity among CAFs, their specific contributions to chemoresistance in gastric cancer (GC) remain incompletely understood. This study identifies THY1 CAFs as a distinct subset associated with poor patient outcomes and oxaliplatin resistance in GC. Both in vitro and in vivo analyses confirmed that THY1 CAFs promote oxaliplatin resistance in GC cells via extracellular vesicles (EVs). Inhibition of EV secretion reduced the chemoresistance-enhancing effects of THY1 CAFs. Proteomic profiling of EVs identified COL11A1 as a protein enriched in THY1 CAF-derived EVs, which was further validated by immunofluorescence and Western blot. Depletion of COL11A1 in THY1 CAF-EVs substantially attenuated their ability to enhance drug resistance in GC cells. High infiltration of COL11A1 and THY1 CAFs was correlated with reduced overall survival and recurrence-free survival in GC patients. RNA sequencing and pathway analysis revealed that THY1 CAF-EVs induce oxaliplatin resistance by activating the PI3K/AKT signaling pathway. Targeting PI3K/AKT signaling counteracted EV-induced chemoresistance, and COL11A1 knockdown in THY1 CAF-EVs reduced PI3K/AKT activation. In conclusion, COL11A1 packaged in THY1 CAF-derived EVs promotes GC chemoresistance via PI3K/AKT signaling, highlighting a potential therapeutic target for overcoming chemoresistance in GC. - Source: PubMed
Publication date: 2026/08/22
Xiong SiZhao ZhenxiongZhang YuGuo Ergang