Anti-Mouse CD47 FITC 50 ug
- Known as:
- Antibody toMouse CD47 fluorecein 50 ug
- Catalog number:
- 11-0471-81
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD47 FITC 50
Related genes to: Anti-Mouse CD47 FITC 50 ug
- 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-Mouse CD47 FITC 50 ug
Related articles to: Anti-Mouse CD47 FITC 50 ug
- Targeting CD47 with monoclonal antibody (mAb) therapy activates tumor-associated macrophages (TAMs). Quantitative imaging methods are important for identifying responders to this novel immunotherapy. The purpose of our study was to investigate whether the metabolic activity of osteosarcomas on F-FDG PET/CT changes after CD47 mAb treatment. Twenty female BALB/c mice with intratibial murine K7M2 osteosarcomas, twenty female NOD scid gamma (NSG) mice with intratibial human 143B tumors, and twenty male NSG mice with intratibial human MG63.3 tumors were treated with either phosphate-buffered saline (PBS) or murine/human CD47 mAb (n = 10 per arm) and underwent either F-FDG PET/CT or ferumoxytol-enhanced MRI (n = 5 per group). Differences in tumor metabolic activity (%ID/g max), tumor T2* relaxation times, TAM (%F4/80), and M1 macrophage polarization (%CD80) between PBS and CD47 mAb-treated mice were estimated from linear regression. The tumor %ID/g max of CD47 mAb-treated K7M2 tumors (6.58 ± 2.42) was not significantly different compared to PBS-treated K7M2 tumors (8.04 ± 2.91; p = 0.17). Similarly, the tumor %ID/g max of CD47 mAb-treated 143B tumors (9.12 ± 1.68) and MG63.3 tumors (5.44 ± 1.99) were not significantly different compared to PBS-treated 143B tumors (9.38 ± 2.32; p = 0.32 ) and MG63.3 tumors (6.02 ± 0.63, p = 0.79 ). By comparison, K7M2 tumors, 143B tumors, and MG63.3 tumors all demonstrated significantly shorter T2* relaxation times after CD47 mAb treatment compared to PBS treatment (all p < 0.001). All tumors exhibited significantly higher TAM (%F4/80) and M1 macrophage polarization (%CD80) after CD47 mAb treatment compared to PBS treatment (all p < 0.05). The metabolic activity of osteosarcomas on F-FDG PET/CT does not show significant changes after CD47 mAb treatment. This lowers the risk of observing pseudoprogression and misinterpreting drug-induced inflammation, simplifying routine clinical scan interpretation. - Source: PubMed
Publication date: 2026/06/05
Roudi RahelehHabte FrezghiSaladino Giovanni MarcoVasyliv IrynaPisani LauraWong JasonSyed AliDaldrup-Link Heike E - Organ shortage remains a major challenge in transplantation medicine. Interspecies blastocyst complementation offers a promising strategy to generate human organs in livestock. However, efficient xenogeneic donor cell engraftment remains challenging. Here, we identify an innate immune barrier wherein host macrophages selectively eliminate viable xenogeneic donor cells, a process we term xenophagocytosis. Mechanistically, xenogeneic cells display elevated phosphatidylserine, an "eat-me" signal recognized by host macrophages through phagocytic receptor Axl. We demonstrate three orthogonal strategies for xenophagocytosis blockade: genetic ablation of macrophages or the Axl receptor in the host embryo or overexpression of the "don't-eat-me" signal CD47 or the phosphatidylserine-regulating flippase ATP11C in donor cells. Xenophagocytosis blockade enhances rat and human donor chimerism in mouse embryos and improves interspecies pancreas complementation efficiency. These findings reveal a previously unrecognized innate immune barrier that safeguards species integrity during early embryogenesis and provide mechanistic insights to enhance xenogeneic chimerism for generating human organs in livestock. - Source: PubMed
Publication date: 2026/06/05
Wang SicongNiizuma KoutaLiu Daniel DanSuchy Fabian PChang Alyssa HTabatabaee SamanSato HideyukiYanagida AyakaMasaki HidekiHidajat NathanHomma ShotaMiyauchi MasashiBhadury JoydeepCharlesworth Carsten TZhang JinyuWeissman Irving LNakauchi Hiromitsu - Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and joint destruction. Efferocytosis is a critical immune process through which the body clears apoptotic cells. Its dysfunction is closely associated with the development of various autoimmune diseases, but its mechanism in RA remains unclear. This study aims to systematically screen candidate biomarkers based on efferocytosis-related genes (ERGs) in RA by integrating bioinformatics and machine learning approaches, and to conduct preliminary validation at both cellular and clinical levels. - Source: PubMed
Publication date: 2026/06/05
Liu Zhenlu - CD47 functions as a "don't eat me" checkpoint, inhibiting macrophage-mediated phagocytosis in triple-negative breast cancer (TNBC). While anti-CD47 therapies can restore immune surveillance, their efficacy in TNBC is often limited by immune evasion and drug development challenges. - Source: PubMed
Publication date: 2026/06/04
Jiang FengjieShen YuLi BingHenry MichaelDavidson NancyHuang Yi - Atherosclerosis is a chronic inflammatory disease characterized by defective efferocytosis, which contributes to necrotic core expansion and plaque instability. This dysfunction arises from two key barriers: first, impaired recognition of apoptotic cells due to activation of the CD47-SIRPα immune checkpoint; and second, insufficient metabolic processing of apoptotic cell-derived substrates, which limits the capacity for continual efferocytosis. Arg1-mediated arginine metabolism has emerged as a crucial pathway supporting this process. To address these limitations, we created Am@SExo, a dual-functional engineered exosome derived from macrophages that unites checkpoint inhibition with metabolic reprogramming. The vesicles overexpress SIRPα on its surface to competitively engage CD47 on apoptotic cells and relieve the inhibitory signal, facilitating initial binding and uptake. Subsequently, it delivers Arg1 mRNA to recipient macrophages, driving an arginine to putrescine program aligned with Rac1 and actin remodeling to sustain successive rounds of clearance. In ApoE mice, systemic administration of Am@SExo significantly reduced necrotic core area, increased fibrous cap thickness, and enhanced features of plaque stability. Together, our findings demonstrate that Am@SExo as a single-platform, dual-phase modulator that restores macrophage continual efferocytosis, offering a promising strategy to resolve inflammation and stabilize atherosclerotic plaques. - Source: PubMed
Publication date: 2026/06/04
Zheng DanwenCai ShitengGao JinfengZhao ShengWei BohanWeng XueyiWang ZhengminWang QiaoziLi QiyuHan ChengzhiLi WeiyanTan YiwenFu YuyuanJi MengHuang ZheyongSong YananQian JuyingGe Junbo