CD63 Clone 'SPM524 antibody Host Mouse
- Known as:
- CD63 Clone 'SPM524 (anti-) Host Mouse
- Catalog number:
- 'AM11115PU-S
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD63 Clone 'SPM524 antibody Host Mouse
Related genes to: CD63 Clone 'SPM524 antibody Host Mouse
- Gene:
- CD63 NIH gene
- Name:
- CD63 molecule
- Previous symbol:
- MLA1
- Synonyms:
- ME491, TSPAN30
- Chromosome:
- 12q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-07
- Date modifiied:
- 2016-01-15
Related products to: CD63 Clone 'SPM524 antibody Host Mouse
Related articles to: CD63 Clone 'SPM524 antibody Host Mouse
- Niemann-Pick disease type C (NPC) is a rare neurodegenerative disease primarily caused by mutations in the gene, which is associated with cholesterol trafficking impairment, and disruption of endolysosomal processing and extracellular vesicles (EVs). Here, for patients with mutations (NPC) and age-matched controls (CTL) we describe the EV profile of dermal fibroblasts ( = 5 NPC, = 3 CTL) and, for the first time, cerebrospinal fluid (CSF, = 5 NPC, = 5 CTL). EVs were enriched using size-exclusion chromatography and characterized by immunoblot, transmission electron microscopy, and microchip resistive pulse sensing. Single vesicle flow cytometry showed increased EV concentration in NPC CSF versus CTLs. In fibroblasts, EV concentration inversely correlated with NPC1 protein levels that was partially attenuated by hydroxypropyl-β-cyclodextrin, an experimental NPC therapeutic. Direct stochastic imaging and multiplexed EV immunoassays revealed that NPC EVs were enriched for endolysosomal proteins (CD63, Lamp1). Three miRNAs (miR-365-3p, -654-3p, -598-3p) were increased in NPC fibroblast EVs and two (miR-320a, -199a/b-3p) in NPC CSF EVs. Pathway analysis using those miRNAs identified relevant diseases and functions (cell death and survival, molecular transport, heredity neurological disease). These results demonstrate that gene mutations alter EV biogenesis and disease-associated changes in cargo that may serve as clinical biomarkers or therapeutic targets for NPC, a devastating disease without a cure. - Source: PubMed
Publication date: 2026/04/17
Hawthorne Sarah Catherine BbSandau Ursula SMcFarland Trevor JBerry-Kravis ElizabethSaugstad Julie A - Extracellular vesicles (EVs) are emerging as diagnostic and therapeutic agents, yet their nanoscale size limits quantitative single-vesicle analysis of surface epitopes and molecular interactions. Flow-Induced Dispersion Analysis (FIDA) is a microfluidic technique enabling real-time measurement of hydrodynamic size and interaction kinetics using fluorescent ligands without requiring surface immobilization. Here, FIDA was applied to characterize EV-antibody interactions using anti-CD63 antibodies across three EV sources: EVs from genetically engineered HEK cells expressing CD63-eGFP or CD63-NeonGreen-Fc domain (CD63-NG-Fc), and EVs from clonally expanded immortalized mesenchymal stromal cells (ciMSCs). FIDA-measured EV diameter sizes ranged from 40 to 90 nm, compared to 70-200 nm as determined by Nanoparticle Tracking Analysis (NTA), likely reflecting methodological differences or NTA's sensitivity to non-EV particles. CD63-binding ECvalues were 1.9 × 10 particles/mL for CD63-eGFP EVs and 8.4 × 10 to 2.4 × 10 particles/mL for ciMSC EVs, indicating higher epitope abundance in engineered vesicles. Within a broader antibody titration, maximal antibody loading to the Fc-receptor domain on EVs was observed at 0.5-5 nM, reaching 30%-40% for IgG1 and 15%-20% for Cetuximab. These results establish FIDA as a high-resolution, label-efficient tool for quantifying EV-antibody interactions and epitope accessibility, supporting its integration into EV standardization and quality control workflows. - Source: PubMed
Kakavoulia Maria-AnthiSpies PeterKutzner Tanja JTertel TobiasFranzmeier SophieAndaloussi Samir ElGiebel BerndKaltner HerbertMeinel DominikGörgens AndréLudwig Anna-Kristin - Extracellular vesicles (EVs) play a pivotal role in cell-cell communication and possess numerous advantages that make them promising candidates for clinical applications. Notably, both natural and engineered small EVs (sEVs) have been widely explored as drug delivery systems (DDSs). However, their short circulating half-life and accumulation in specific organs remain major obstacles to therapeutic use, primarily due to immune clearance by the mononuclear phagocyte system (MPS). In this study, we demonstrate that a truncated form of CD63 directs the sorting of a chimeric CD47-CD63 protein into sEVs. The extracellular domain of CD47 binds to signal regulatory protein α (SIRPα), activating the phagocytic "do not eat me" signal. The sEVs enriched with the chimeric CD47-CD63 protein effectively evade phagocytosis by activated macrophages . Additionally, CD47-CD63 significantly reduces the uptake of sEVs by blood-derived mononuclear phagocytes . CD47-CD63 enrichment in sEVs markedly prolongs their circulating half-life and reduces their accumulation in the liver, spleen, and lungs. These findings suggest that the chimeric CD47-CD63 protein confers immune evasion properties to sEVs and provides a promising strategy to overcome the current limitations of sEV-based therapeutic applications. - Source: PubMed
Publication date: 2026/04/16
Tang ShuangshuangLiu ShilinWang MeilinShen TianyuWang DekunMi XueZhang YuyingZhang MiaoPan LeitingTan XiaoyueJiang ChunyangYue Shijing - - Source: PubMed
Publication date: 2026/04/16
Chen SiyuWang FeifanChen CongCheng YangjianChen MingliangLi ZengpengTang Xixiang - Microbial-driven spontaneous preterm birth (sPTB) is linked to adverse vaginal microbiome and dysregulated immune responses, yet this knowledge has not translated into predictive tools or therapies. We sampled 186 high-risk pregnant women and assessed 14 complement proteins and the neutrophil immunophenotype at the cervicovaginal interface to expand potential targets. Alterations in classical and alternative complement pathway components were associated with bacterial community composition and preceded cervical shortening and sPTB. At 12-16 weeks, women with Community State Type (CST) IV had significantly higher concentrations of C1q, C4, C4b, Factor B, D, C3b/iC3b, and Factor H, I than those with CST I. Women who later developed a short cervix and delivered preterm showed lower L. crispatus abundance and elevated complement activation. Neutrophils were the dominant local immune cell and exhibited enhanced activation relative to peripheral neutrophils, with altered expression of CD11b, CD62L, CD63 and CD66b. Cervical neutrophil CD63, CD66b, and CD88 differed between CST IV and CST I, though not by pregnancy outcome. Neutrophil abundance correlated with cytokines, complement proteins, and MMPs, suggesting roles in inflammation and tissue remodelling. These findings highlight a microbiota-driven complement-neutrophil axis present before cervical remodelling and sPTB, identifying potential complement-based predictors and therapeutic targets. - Source: PubMed
Publication date: 2026/04/15
Gimeno-Molina BelenCorreia Gonçalo Dos SantosNg SherrianneLee Yun SBayar ErnaLove Ryan LZhao SihaoMountain Katherine ETeoh T GBrown Richard GDavid Anna LLewis Holly VTerzidou VassoBotto MarinaKropf PascaleMacIntyre David ABennett Phillip RSykes Lynne