Anti-Human CD47 FITC 25 tests
- Known as:
- Antibody toHuman CD47 fluorecein 25 tests
- Catalog number:
- 11-0478-71
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD47 FITC 25 tests
Related genes to: Anti-Human CD47 FITC 25 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 25 tests
Related articles to: Anti-Human CD47 FITC 25 tests
- 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-SIRPĪ± 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 SIRPĪ± 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 - Gastric cancer remains a leading cause of cancer-related mortality worldwide, with high metastatic potential being a critical factor for poor prognosis. Notably, the objective response rate (ORR) of current immunotherapies, such as immune checkpoint inhibitors (ICIs), remains below 20%. Within the tumor microenvironment (TME), the dynamic interactions among immune cells profoundly regulate tumor progression, in which the remarkable plasticity of tumor-associated macrophages (TAMs) plays a pivotal role. Under the induction of microenvironmental signals, TAMs can polarize into either the anti-tumor M1 phenotype or the pro-tumor M2 phenotype. This review summarizes the research progress of macrophage polarization in distant metastasis of gastric cancer, with a specific focus on the regulatory mechanisms of core signaling pathways, including STAT3, PI3K/AKT, and exosomal ncRNA regulatory networks, in macrophage functional reprogramming and metastatic niche formation. Furthermore, we discuss potential immunotherapy strategies centered on modulating macrophage phenotypes, such as CSF1R inhibitors, CD47 blockers, and their combination with ICIs. These findings provide a significant foundation for developing macrophage-targeted therapeutic interventions, screening translational biomarkers, and improving the prognosis of patients with metastatic gastric cancer. - Source: PubMed
Publication date: 2026/06/04
Gong NingningQin GuanminSun JunxiaShen ShiyingZhang XinxingLu Minmin - Hepatic ischemia-reperfusion injury (HIRI) is clinically linked to post-transplant complications, yet the pathogenic role of programmed cell death (PCD) patterns in this process remains poorly delineated. This study aimed to investigate the diversity of programmed cell death (PCD) patterns underlying HIRI, with a focus on mechanistically dissecting macrophage-hepatocyte crosstalk mediated by the THBS1-CD47 axis. - Source: PubMed
Publication date: 2026/05/19
Xie ManlingZhang ChangquanZhu LirongPei YongfengLiang ChunyanFu LixinLi HaibinLan LiugenWen NingWu JihuaSun Xuyong