CD63
- Known as:
- CD63
- Catalog number:
- 1P-343-T025
- Product Quantity:
- 25 tests
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD63
Related genes to: CD63
- 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
Related articles to: CD63
- The arthritogenic alphavirus chikungunya virus (CHIKV) causes debilitating long-lasting joint pain. Host factors used by CHIKV to infect joint cells are largely unknown. Here, we evaluated the role of the 19 tetraspanins expressed in primary human synovial fibroblasts in virus infection. The exosome-associated tetraspanins CD63, CD9, and CD151 supported CHIKV infection of joint fibroblasts. Silencing of CD63 and CD151 reduced subgenomic replicon activity. CD9 localized in close proximity to replication sites and its silencing reduced intracellular CHIKV genome accumulation. Silencing of all three tetraspanins reduced progeny virus production. While these tetraspanins were dispensable for CHIKV entry into joint fibroblasts, the receptor MXRA8 promoted cell entry. Our findings demonstrate that CHIKV exploits tetraspanins as host factors in synovial fibroblasts, shedding light on molecular mechanisms underlying CHIKV pathogenesis in joint tissues. - Source: PubMed
Publication date: 2026/09/26
Brown Eve KStegmann CoraBiermann HannahPittl VerenaDuven Marade Bruin Anja C MNeumann ElenaGerold Gisa - Bleeding in Gaucher disease (GD) is not fully explained by thrombocytopenia and coagulation disorders. Previous studies have shown impaired agonist-induced cluster of differentiation (CD) 62P (CD62P/P-selectin) responses, but their persistence over time is unknown. This retrospective longitudinal observational study characterized platelet activation and secretion responses over time and factors associated with persistent abnormalities. Whole-blood flow cytometry studies from 333 patients with GD with at least two assessments were analyzed. Platelet activation complex-1 (PAC1), CD62P, and CD63 responses were categorized longitudinally. Patients contributed 949 visits over a median follow-up of 2.3 years. Persistent CD62P abnormality was most frequent (92/333, 27.6%), compared with PAC1 (45/329, 13.7%) and CD63 (9/328, 2.7%). PAC1 abnormalities were more often dynamic, whereas CD62P abnormalities were frequent and persistent, most often involving thrombin receptor-activating peptide 6 (TRAP-6) and cross-linked collagen-related peptide (CRP-XL). Lower platelet count was independently associated with persistent CD62P abnormality, although approximately half of affected patients had platelet counts ≥150 × 10/L. Treatment throughout follow-up was associated with lower odds of persistent CD62P and CD63 abnormalities. Impaired CD62P expression was the predominant persistent abnormality, consistent with preferential impairment of α-granule secretion. Platelet function changed over time, supporting reassessment in patients with bleeding manifestations and before procedures when previous testing is remote or clinical status has changed. - Source: PubMed
Publication date: 2026/09/16
Revel-Vilk ShoshanaZimran AriDinur TamaFrydman DafnaShulman ElenaBenayoun EmmanuelBroide EtiNaamad MiraKoren NechamaSaltsman Michal - Tofacitinib is a Janus kinase inhibitor used to treat inflammatory diseases, including rheumatoid arthritis and ulcerative colitis (UC). Previous studies have reported an increased risk of thromboembolic events in patients with rheumatoid arthritis treated with tofacitinib. Therefore, evaluating whether these effects are also present in other inflammatory diseases such as UC is important. - Source: PubMed
Publication date: 2026/09/10
Suarez-Trujillo FabioMartínez Paula JSoleto IreneMeijón MarKerguelen AnaOrts MarPlanas AntonioAcedo NataliaChacón-Calvo GuillermoGarre AnaMoreno-Lopez ElenaButta NoraChaparro MaríaBaldán-Martín MontseGisbert Javier P - Multiplexed protein profiling of single extracellular vesicles (EVs) is crucial for precise liquid biopsy but is severely limited by steric hindrance arising from bulky detection probes. This study systematically deconstructs the sources and consequences of this limitation using high-sensitivity nano-flow cytometry (nFCM), revealing how the spatial footprint of antibody-fluorophore conjugates fundamentally compromises co-detection fidelity. To overcome this, we developed a sterically optimized framework through the sequential minimization of the spatial footprint of detection elements: first, by replacing large fluorophores with compact organic dyes and, most effectively, by employing nanobodies. This approach significantly enhanced the detection of dual-protein-positive EV subpopulations by mitigating mutual steric interference. Notably, the persistent labeling limitation observed for closely apposed protein pairs, such as CD9/CD63, was repurposed as a sensitive probe for inferring nanoscale membrane topography. Clinically, simultaneous dual-nanobody detection of PD-L1 and CD47 on plasma-derived EVs achieved an overall accuracy of 90.0% for breast cancer diagnosis. This work establishes a generalizable framework for accurate, multiplexed EV profiling in clinical diagnostics. - Source: PubMed
Publication date: 2026/09/22
Hu YunyunDi HaonanLin LinjunKang ZuzheChen JunyanTian YeLi ZengpengYan Xiaomei - Hepatocellular carcinoma (HCC) progression involves epithelial-mesenchymal transition (EMT) and glycolytic reprogramming induced by TGF-β1. The role of exosomal circular RNAs in coordinating these processes remains unclear. This study aims to investigate whether exosomal circ-ZNF652 is associated with TGF-β1-induced mesenchymal marker induction and glycolysis in HCC and elucidate the underlying mechanism. Exosomes were isolated from SMMC-7721 cells and characterized by TEM, NTA, and CD63 western blot. RT-qPCR measured circ-ZNF652 expression. Cell viability, migration, cycle, and apoptosis were assessed by MTT, wound healing, and flow cytometry. EMT and glycolysis proteins were detected by western blot. Glucose uptake, lactate, and HK/LDHA activities were measured. xenograft and rescue experiments with AKT/HIF-1α inhibitors were performed. TGF-β1 stimulation upregulated circ-ZNF652 in SMMC-7721 cells and their exosomes. Exosomal circ-ZNF652 was internalized by HCC cells and further enhanced TGF-β1-induced upregulation of EMT markers (Twist1, N-cadherin, vimentin, MMP-9). It also promoted cell proliferation, migration, S-phase entry, reduced apoptosis and Caspase-3 activity. Moreover, Exos circ-ZNF652 augmented TGF-β1-induced glycolysis as evidenced by increased glucose uptake, lactate secretion, HK/LDHA activities, and Glut-1/HIF-1α expression. , circ-ZNF652 overexpression significantly increased tumor volume (1286.5 vs 452.8 mm) and weight (1.32 vs 0.48 g), along with elevated Ki-67, N-cadherin, HIF-1α, and p-AKT. Rescue experiments showed that AKT or HIF-1α inhibition reversed circ-ZNF652-mediated EMT and glycolysis. All differences were statistically significant (<0.05). To sum up, exosomal circ-ZNF652 is associated with TGF-β1-induced mesenchymal phenotype acquisition and glycolysis via the AKT/HIF-1α pathway, promoting HCC progression. It represents a potential non-invasive biomarker and therapeutic target for HCC. - Source: PubMed
Publication date: 2026/09/02
Niu XianliZhang XiaominLiang GuangxiaWei NinaPeng HaiboLi Xiangyang