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
Ask about this productRelated 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
- Plasma membrane lipid asymmetry is tightly regulated and fundamental to mammalian cell physiology. TMEM30A is the β-subunit of P4-ATPases, flippase enzymes that maintain strict phosphatidylserine (PS) asymmetry by pumping it from the outer to the cytosolic leaflet. Loss of TMEM30A function causes constitutive PS externalization and has been implicated in diseases such as diffuse large B-cell lymphoma and tumor immune evasion. Here, we systematically define the biophysical and molecular consequences of TMEM30A deletion in immune cells. Using a live-cell lipid reporter, membrane order probe, and surface proteome mapping, we show that TMEM30A-knockout cells display robust PS externalization accompanied by faster lateral diffusion of membrane constituents and decreased plasma membrane order. Surface proteome reorganization includes increased abundance of tetraspanins and CD47. Furthermore, TMEM30A loss triggers glycocalyx remodeling via ADAM10-dependent shedding, which removes major transmembrane mucins, including CD43 and CD162 (also known as SPN and SELPLG, respectively). Together, these data reveal a coordinated reorganization of lipids, glycans and proteins upon TMEM30A loss, suggesting mechanistic links between flippase dysfunction and increased plasma membrane dynamics and potential sensitization to immune therapy. Furthermore, our study provides an integrated surfaceome framework that might shed light on the relationship between TMEM30A expression and clinical outcomes in cancer. - Source: PubMed
Publication date: 2026/08/14
Gurdap Cenk ORagaller FranziskaMuller MarionSjule EllenSych TarasBlomén LinneaThorén Fredrik BLevental IlyaLevental Kandice RSattentau Quentin JSezgin Erdinc - Smoking cessation decreases lung cancer progression; however, its effects on precancerous lesions and the underlying mechanisms remain unclear. This study established a mouse model of precancerous pulmonary nodules and employed single-cell RNA sequencing (scRNA-seq) and immune repertoire sequencing (IR-seq) to elucidate the regulatory mechanisms by which smoking cessation influences the development of lung precancerous lesions. - Source: PubMed
Publication date: 2026/08/13
Wang XintongTang FangQin JiayuXiao TiquanShi LiweiZhang ShujunChe Chunli - Atherosclerosis is one of the leading causes of death worldwide. Excessive lipid accumulation and defective efferocytosis trigger massive foam cell formation, which serves as a key driver of atherosclerotic plaque progression. In this work, we developed a phospholipid-based nanocarrier (Ato@LHP) to co-load atorvastatin and a CD47-blocking peptide. This system achieves targeted treatment of atherosclerosis through lipid removal and dual CD47 blockade. We used RAW264.7 cells to build foam cell models , characterized the physicochemical properties of the nanocarrier, and verified its plaque-targeting ability. Six-week-old male ApoE/ mice were fed a high-fat diet for 8 weeks to establish aortic atherosclerosis models, and then were randomly divided into four groups: Saline, Ato@L, Ato@LH, and Ato@LHP. results showed that compared with the Saline group, Ato@LHP treatment reduced aortic plaque area percentage from 28.8% to 11.1%, and the plaque vulnerability index simultaneously decreased from 1.14 ± 0.05 to 0.55 ± 0.04. Mechanistic studies indicated that atorvastatin acts through an endogenous pathway: it blocks the nuclear translocation of NF-κB p50 and reduces CD47 gene transcription. Meanwhile, the nanocarrier responds to reactive oxygen species (ROS) at lesion sites and releases Pep-20 (a CD47-blocking peptide), which directly blocks the CD47/SIRPα interaction an exogenous pathway. These two pathways work together to restore macrophage efferocytosis and accelerate the clearance of apoptotic foam cells. In addition, Ato@LHP clearly reduces lipid accumulation in plaques, relieves local inflammation, and stabilizes atherosclerotic plaques. This strategy of combining dual CD47 blockade with targeted lipid clearance offers a reliable new approach for targeted atherosclerosis treatment. - Source: PubMed
Publication date: 2026/07/30
Yuan PengTian ShiboCui ChaoSun ChengluTang ChuangGao DengfengLu LuLong KerenXu FunengShu GangZhang WeiLiang XiaoxiaKong FanliLi MingzhouLi Haohuan - Esophageal carcinoma (ESCA) remains highly lethal and lacks robust biomarkers for early detection and risk stratification. High mobility group box 3 (HMGB3) has been implicated as an oncogene in several cancers, but its role in ESCA has not been fully defined. To address these clinical and biological gaps, this study systematically characterized the expression profile, diagnostic and prognostic value, biological functions, and immune-related features of HMGB3 in ESCA through integrative bioinformatics analyses and validation. - Source: PubMed
Publication date: 2026/06/24
Fu Shen-BoJin LongLiu JiaYang RongLiang JingGuo Jun-JunChen LiZhao Bin - Milk-derived extracellular vesicles (EVs) transport microRNAs (miRNAs) that are unusually stable and have been proposed to survive digestion and modulate gene expression in the consumer, although their dietary bioavailability and physiological relevance remain debated. How the predicted regulatory potential of these miRNAs differs among the milks of different animals most relevant to human nutrition has not been systematically compared. Here, we performed an integrative in silico analysis of publicly available small-RNA sequencing data from 29 milk and milk-cell samples of human, cow, goat, and donkey origin. miRNAs were quantified against human (hsa) miRBase references-thereby restricting the analysis to evolutionarily conserved miRNAs with human orthologs-and their predicted effect on the human transcriptome was modeled by integrating predicted (mirDIP database) and experimentally supported (TarBase v9 database) miRNA-target interactions into a per-gene, per-species weighted targeting score. Because miRNAs act predominantly as repressors, this score is read as a prediction of which genes would be post-transcriptionally down-regulated in a recipient. miR-148a-3p dominated the exosomal spectrum of all four species (human, cow, goat, and donkey; ≈21.5% of pooled abundance), and the twenty most abundant miRNAs accounted for roughly three quarters of the signal. Of 4577 robustly targeted genes, a 1809-gene conserved "pan-milk" core showed the highest cross-species targeting and was enriched for transcriptional regulation, PI3K-Akt, MAPK, and TGF-β/SMAD signaling, autophagy and-strikingly-the components of the RNA-interference machinery itself. Species-restricted gene sets recapitulated biologically plausible programs, including a human-biased neuronal/axon-guidance and chromatin module, a donkey-biased transcriptional, epithelial, and immune () module, and a ruminant lipid/cholesterol and insulin-mTOR module. Across categories, we observed a reproducible confidence-exclusivity trade-off. We emphasize that these results are computational predictions that assume dietary miRNA uptake and do not constitute experimental validation. We provide the complete targetome as a hypothesis-generating resource to prioritize candidate genes, pathways, and milk types for future functional, nutritional, and epigenetic investigation. Across the 29 samples from the four species, miRNA composition segregated by species (silhouette width = 0.82, a cluster-separation measure ranging from -1 to 1, with values near 1 indicating well-separated groups) and the category structure exceeded a permutation null, indicating that the between-species signal is robust to differences in dataset origin and milk state. - Source: PubMed
Publication date: 2026/08/02
Zoziuk MaksymDjibagaou Abel DafogoTerrinoni AlessandroKoroliouk DimitriColizzi Vittorio