CD63
- Known as:
- CD63
- Catalog number:
- 1P-343-T100
- Product Quantity:
- 100 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
- To investigate the effects of adipose tissue-derived extracellular vesicles (AT-EVs) on zoledronic acid (ZA)-induced impairment of proliferation, migration, osteogenic differentiation and apoptosis of bone marrow mesenchymal stem cells (BMSCs), and to preliminarily explore the underlying molecular mechanisms. AT-EVs were isolated from subcutaneous adipose tissue of 4-week-old male SPF SD rats, and characterized by transmission electron microscopy, nanoparticle tracking analysis and Western blotting; the uptake of AT-EVs by BMSCs was observed. BMSCs derived from the femurs and tibias of rats of the same batch were isolated and cultured, and identified by flow cytometry and tri-lineage differentiation. The working concentration of ZA was screened by cell counting kit-8 (CCK-8). BMSCs were divided into control, ZA (5 μmol/L), and ZA+AT-EVs (5 μmol/L ZA+50 μg/ml AT-EVs) groups; proliferation was evaluated by CCK-8 combined with 5-ethynyl-2'-deoxyuridine (EdU) incorporation assay, and migration was evaluated by wound healing and Transwell assays; for the apoptosis assay, 10 μmol/L ZA was applied and detected by flow cytometry after Annexin V/PI staining. The osteogenic differentiation experiment included five groups (Control, Osteogenic induction, Osteogenic induction+AT-EVs, ZA, and ZA+AT-EVs), in which alkaline phosphatase (ALP) staining and Alizarin red S staining were performed, mineralized nodule formation was quantified by the cetylpyridinium chloride decolorization method, and the mRNA expression of Runx2, ALP and OCN was detected by real-time quantitative PCR. Cells from the ZA and ZA+AT-EVs groups after 7 days of osteogenic induction were subjected to liquid chromatography-tandem mass spectrometry-based proteomic analysis, followed by principal component analysis, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. AT-EVs exhibited a cup-shaped bilayer membrane structure with a peak diameter of 116.8 nm, were positive for CD9, CD63 and CD81 and negative for Calnexin, and were efficiently taken up by BMSCs. CCK-8 results showed that 5 μmol/L ZA significantly inhibited BMSCs proliferation (<0.001), and AT-EVs partially restored the proliferation capacity. The EdU incorporation assay further showed that, compared with the Control group, the EdU-positive rate of the ZA group was significantly decreased (<0.001), while that of the ZA+AT-EVs group was significantly increased compared with the ZA group (<0.01), consistent with the CCK-8 results. Compared with the ZA group, the ZA+AT-EVs group showed enhanced BMSCs migration (all <0.05) and a significantly reduced total apoptosis rate (<0.001). Western blotting further showed that AT-EVs down-regulated the ZA-induced elevation of cleaved caspase-3 (<0.001) and BAX (<0.01) and up-regulated Bcl-2 expression. AT-EVs significantly ameliorated the ZA-induced suppression of BMSCs ALP expression and mineralized nodule formation (<0.001). qPCR showed that AT-EVs up-regulated the ZA-suppressed expression of Runx2, ALP and OCN (<0.05), whereas no significant difference was found between the Osteogenic induction+AT-EVs group and the Osteogenic induction group. Proteomic analysis identified 483 differentially expressed proteins (344 up-regulated and 139 down-regulated), which were mainly enriched in steroid biosynthesis, the cGMP-PKG signaling pathway and cytoskeleton regulation pathways. AT-EVs can effectively ameliorate the ZA-induced impairment of proliferation, migration and osteogenic differentiation of BMSCs and reduce apoptosis in vitro, and their effects may be related to the overall down-regulation of steroid biosynthesis pathway-related proteins and the predominant up-regulation of cGMP-PKG signaling pathway-related proteins in the ZA+AT-EVs group. - Source: PubMed
Publication date: 2026/09/30
Sun X YPan Z JCao Z WZhou X XWang LHong P YPan J - Platelet protease-activated receptors (PAR)1 or PAR4 can be specifically activated with thrombin receptor-activating peptides, available with either amide (-NH), or free-acid (-OH) in their C-terminus. - Source: PubMed
Publication date: 2026/09/29
Boukhatem ImaneBlais Jessicavan der Wal Dianne EBaloch HannaJerlström TeaLordkipanidzé MarieRamström Sofia - Programmed death-ligand 1 (PD-L1) undergoes continuous endocytosis and post-endocytic sorting that determine its recycling to the plasma membrane, lysosomal degradation, and exosomal secretion. Although PD-L1 internalization depends on RAB5-mediated endocytosis, whether canonical autophagy contributes to the subsequent sorting of internalized PD-L1 remains unclear. Here, we show that canonical autophagy is dispensable for the post-endocytic fate of cell-surface PD-L1. Genetic disruption of core autophagy components, including LC3B, ATG4B, ATG5, and ATG7, did not impair delivery of internalized PD-L1 to early endosomes, multivesicular bodies (MVBs), late endosomes, or extracellular vesicles. Pharmacologic inhibition of autophagosome-lysosome fusion increased PD-L1 accumulation in RAB5- and CD63-positive compartments, but this effect persisted in cells lacking LC3B, ATG5, or ATG7, further indicating that canonical autophagy is not required for PD-L1 endosomal sorting or exosomal secretion. Instead, we identify CAPZ, a CAPZα-CAPZβ heterodimer best known for actin filament capping, as a regulator of PD-L1 post-endocytic sorting. Loss of CAPZ reduced PD-L1 delivery to CD63-positive MVBs and incorporation into exosomes while increasing its accumulation in RAB11-positive recycling endosomes, resulting in elevated cell-surface PD-L1. Functionally, CAPZ-deficient tumor cells were less sensitive to peripheral blood mononuclear cell-mediated killing, consistent with increased surface PD-L1 and enhanced immune-evasive capacity. Together, these findings indicate that CAPZ-dependent endosomal maturation controls the balance between PD-L1 recycling and MVB/exosomal sorting independently of canonical autophagy, thereby influencing PD-L1 surface abundance and tumor immune evasion. - Source: PubMed
Publication date: 2026/09/29
Xu PengYe ZuodongZhu YanniChan Chuen-FukLi YanhuaHuang HuiruZhu ChengyiZhang XiaoyinWang YijingWang YilinLin NaixinSun WeiPeng MeiyuLu YingyingYue Jianbo - Basophils are recognized as important effector cells during the sensitization and effector phases of IgE-mediated allergy. Besides histamine release during anaphylaxis, basophils contribute to early immune polarization as an important source of Th2-associated cytokines. Vespula spp. venom immunotherapy (VIT) represents a prime example of clinically highly effective allergen-specific immunotherapy. This study investigated functional and phenotypic changes in circulating basophils during early VIT in a homogenous case series. - Source: PubMed
Publication date: 2026/09/24
Fleissner JanikStoevesandt JohannaGoebeler MatthiasTrautmann AxelKerstan Andreas - 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