Anti-Human CD47 FITC 100 tests
- Known as:
- Antibody toHuman CD47 fluorecein 100 tests
- Catalog number:
- 11-0479-42
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD47 FITC 100 tests
Related genes to: Anti-Human CD47 FITC 100 tests
- Gene:
- CD47 NIH gene
- Name:
- CD47 molecule
- Previous symbol:
- MER6
- Synonyms:
- IAP, OA3
- Chromosome:
- 3q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-12
- Date modifiied:
- 2016-10-05
Related products to: Anti-Human CD47 FITC 100 tests
Related articles to: Anti-Human CD47 FITC 100 tests
- Platelets have been increasingly recognized as versatile regulators of ageing, immunity, and cancer, yet their functional heterogeneity has remained poorly defined. We performed the first large-scale single-cell RNA sequencing of 28,192 platelets from healthy, aged, metastatic, and treated mice using the BD Rhapsody platform. Our analysis revealed four conserved and functionally distinct platelet transcriptional states: haemostatic platelet (HP), neural gene-enriched platelet (NEP), platelet-leukocyte aggregate (PLA) and platelet-erythrocyte aggregate (PEA). Among these states, Tpm2-high HP is linked to ageing-associated lung metastasis and is characterized by cytoskeletal remodelling gene signatures. The PLA state was predicted to be a signalling hub for immunothrombosis, with a PLA-Bridge subpopulation coordinating immune-adherent platelets via the Ppbp-Cxcl2 and Thbs1-Cd47 checkpoint axes. Strikingly, AAV-mPf4 gene therapy was associated with a neural gene-enriched platelet-associated transcriptional program, which mitigates age-related functional decline. This study provides a single-cell transcriptomic atlas of murine platelets under ageing and metastasis conditions and reveals transcriptional state-specific heterogeneity. This study also proposes PF4-based interventions and cytoskeletal candidates for diagnosis and therapy. - Source: PubMed
Publication date: 2026/08/11
Li RunzeChen YuyiSong YuanyuanZhang AoLiang TuliangLian LirongMi JianingZhou NanjieWang JingrongBai YingnanPan HudanLiu QuanZhao YichengLiu Liang - Atherosclerosis (AS) is a chronic inflammatory disease characterized by plaques that are difficult to eliminate. Neutrophil extracellular traps (NETs) are a central factor in the progression of AS, which could trigger a cascade of inflammatory reactions and increase plaque volume. Focusing on inhibiting the release of NETs within plaques is beneficial for erasing plaques. However, the arterial stenosis and poor blood flow caused by plaques prevent most therapeutic agents from entering the AS lesions. Considering that activated neutrophils firstly migrate to the interior of plaques after being stimulated by cytokines, we proposed a strategy based on bacteria-derived outer-membrane vesicles (OMVs) to hitchhike activated neutrophils for enhancing AS plaques delivery of therapeutic agents to treat AS. DNase Ⅰ and atorvastatin (At) were encapsulated into OMVs to prepare OMV@DAt nanoparticles, which could be specifically internalized by activated neutrophils in blood circulation by inheriting analogous functions to the bacterial outer-membrane. Neutrophils endocytosed OMV@DAt could infiltrate into the AS plaques to boost drugs concentrations. OMV@DAt was certified to significantly degrade NETs from neutrophils and inhibit the expression of CD47 in apoptotic cells, which could further alleviate the inflammatory response, enhance the clearance of lipid necrotic cores by macrophages, and ultimately promote plaque regression. - Source: PubMed
Publication date: 2026/08/06
Liu MinLiu SiyiYang HanSun YatingZhao GuanxinXiu JingyaZhang JiulongZhao Xiuli - Blocking the CD47-SIRPα checkpoint reactivates macrophage-driven elimination of malignant cells, although CD47 antagonists have progressed substantially in clinical trials, their implementation is hindered by on-target hematologic toxicity, particularly unintended binding to red blood cells (RBCs). The present study was therefore undertaken to develop a humanized anti-CD47 antibody that achieves robust antitumor activity with an enhanced safety margin. - Source: PubMed
Publication date: 2026/08/11
He MingxiaZhao YaoyaoCao JiujiuLi ZhongdaoWang LihaoHou SiyuanZhang QiangjianSun LiangZhao YuqiChen TianyuGuo ZhigangJu Dianwen - Red blood cell (RBC)-based therapeutic enzyme delivery systems require cell sources that can support future standardized large-scale production, with the prerequisite that engineering modifications preserve the cells' inherent biocompatibility and long-circulating potential. In this study, we first demonstrated proof-of-principle by successfully engineering asparaginase (ASPG)-loaded erythroid cells in the human erythroid progenitor cell line (HUDEP-2), where efficient ASPG expression and intact enzymatic activity were confirmed. To facilitate clinical translation, the validated strategy was further applied to human induced pluripotent stem cells (iPSCs), and the differentiated products were systematically characterized. It is worth noting that the key membrane markers of iPSC-derived ASPG-loaded erythroid cells (i-ASPG-R), including CD47 and CD55, were comparable to those of human RBCs (hRBCs). The results of Annexin V staining indicated a healthy cell status. More importantly, these cells displayed ASPG activity equivalent to that of HUDEP-2-derived counterparts. Moreover, the expression of ASPG did not affect enucleation and the composition of globin. In vitro function assays showed that compared with the control group, the proliferation of CCRF-CEM leukemia cells was inhibited by 48% after 24 h of co-culture with i-ASPG-R. In summary, this study established an iPSC-derived platform for generating ASPG-loaded erythroid cells with favorable carrier properties and evident anti-leukemic activity in vitro, laying a conceptual foundation for future cell therapy manufacturing via optimized terminal maturation. - Source: PubMed
Publication date: 2026/08/08
Cheng XiaobeiZhang BiaoLing YamengDeng HuiziYang YangXi JiafeiYang MeiyanGong WeiWang YuliYue WenLi YiGao Chunsheng - Genetically engineered porcine red blood cells (pRBCs) are emerging as a potential supplementary source of oxygen-carrying cells for transfusion medicine. Triple-knockout (TKO) pigs lacking major carbohydrate xenoantigens, including Gal, Neu5Gc, and Sd(a), have substantially reduced human antibody binding in vitro, and additional expression of human protective molecules such as CD55 and CD47 may further improve compatibility. However, the translational development of pRBC xenotransfusion is now constrained less by donor engineering alone than by the absence of an appropriate in vivo evaluation model. Old World nonhuman primates have historically served as essential preclinical models in xenotransplantation, but their cytidine monophosphate-N-acetylneuraminic acid hydroxylase (CMAH)-positive background and natural antibody repertoires may exaggerate immune barriers to TKO pRBCs that are not fully representative of humans. New World nonhuman primates, brain-dead human models, and eventually carefully regulated early-phase human studies each offer distinct advantages and limitations. In this Commentary, we argue that pRBC xenotransfusion requires a purpose-specific translational framework rather than reliance on a single preclinical model. Such a framework should integrate standardized compatibility testing, in vitro human assays, animal-based safety stress-testing, and, where ethically and legally feasible, short-term human reference models. - Source: PubMed
Publication date: 2026/08/06
Lei XiayuHara HidetakaLi TaoWang Yi