Proteins CD47 , Human
- Known as:
- Proteins CD47 , Human
- Catalog number:
- C321
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins CD47 Human
Related genes to: Proteins CD47 , Human
- 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: Proteins CD47 , Human
Related articles to: Proteins CD47 , Human
- Mycosis fungoides (MF) is the predominant subtype of cutaneous T-cell lymphoma, whereas large plaque parapsoriasis (LPP) closely resembles early-stage MF, making differential diagnosis challenging. Immune markers, such as CD47, CD163, and B7-H3, play crucial roles in tumor immune evasion and macrophage polarization. However, their expression profiles and potential diagnostic or prognostic implications in early-stage MF and LPP remain poorly defined. Therefore, this study aimed to evaluate the expression of CD47, CD163, and B7-H3 in early-stage MF and LPP and analyze their associations with clinicopathological characteristics and patient outcomes. This retrospective study evaluated the immunohistochemical expression of CD47, CD163, and B7-H3 in 46 patients with early-stage mycosis fungoides (MF) and 46 patients with large plaque parapsoriasis (LPP). Expression levels were assessed using an immunoreactivity scoring system and analyzed for their associations with clinical parameters and disease-free survival (DFS). The study included patients diagnosed and followed at Sivas Cumhuriyet University between 1 March 2015 and 31 March 2025. : High CD47 expression was detected in 72.7% of MF patients, high B7-H3 expression in 45.7%, and high CD163 expression in 46.7% compared with LPP patients ( < 0.001). These markers showed positive correlations, and elevated expression, especially of B7-H3 and CD163, was associated with shorter disease-free survival in univariate analysis. : The higher expression of CD47, CD163, and B7-H3 in early-stage MF compared with LPP suggests that these markers may contribute to the differential diagnosis and could represent potential therapeutic targets; however, their independent prognostic value requires confirmation in larger studies. - Source: PubMed
Publication date: 2026/04/02
Yasak Guner RukiyeYüceer Ramazan OguzUnsal Ahmet Turan - Immunotherapies have shown promise effectiveness in cancer treatment, yet the complex tumor microenvironment poses challenges to their efficacy. The interaction between immune checkpoints in malignant and immune cells is crucial for cancer cells to evade the host's immune response, but the impact of tumor cell immune checkpoint molecules on disease progression remains incompletely understood. Our study uncovers a significant link between the CD47 signals, inflammasomes and intestine-specific homeobox (ISX), correlating strongly with lesion count, disease stage, and lymph vascular invasion. Elevated CD47 expression activates CD47-SIRPα signaling to promote M2-like macrophage polarization, accompanied by inflammasome activation and cytokine production within the tumor microenvironment and memory T cell differentiation within the hepatic microenvironment, intensifying disease progression. In xenograft and chronic hepatic tumor model featuring a liver-specific ISX mutant, the elimination of M2-like TAM macrophages and TRM cells halts disease advancement. Through transcriptomic analysis and molecular evidence, we unveil the interaction of ISX with TWIST1, triggering CD47-SIRPα and inflammasome activation by binding to specific degenerate sequences ("-GGDWYR-") in the promoter regions of CD47-SIRPα signals and inflammasome-related genes. These findings underscore the pivotal role of the ISX-CD47 axis in liver disease and tumor progression. They offer promising insights into potential treatments for liver disease, shedding light on new therapeutic strategies with the potential to improve patient outcomes. - Source: PubMed
Publication date: 2026/05/04
Wang Li-TingLin Ming-HongLi Yi-ChuanWang Shen-NienChai Chee-YinHsu Jung-MaoChiou Shyh-ShinChiou Hsin-Ying ClairHuang Shau-KuHung Mien-ChieHsu Shih-Hsien - The pathogenesis of atherosclerosis involves a vicious cycle characterized by abnormal cholesterol crystals (CCs) accumulation, chronic inflammation, and endothelial dysfunction. CCs accumulation triggers chronic inflammation, which subsequently damages the endothelium, thereby exacerbating lipid leakage and further CCs deposition. Disrupting this pathological cycle is an urgent therapeutic challenge. Our study identified the cGAS-STING signaling pathway-known for mediating DNA immune sensing-as being closely associated with lipid deposition, endothelial dysfunction, and inflammation in atherosclerosis. Furthermore, we investigated the therapeutic potential of lipid micelles composed of lecithin and DSPE-PEG conjugated with a CD47-targeting peptide. These micelles were loaded with methyl-β-cyclodextrin (MCD) and polyhistidine inclusion complexes (PLCH micelles) for dissolving CCs and treating atherosclerosis. PLCH micelles achieve targeted delivery to apoptotic foam cells via the CD47-targeting peptide. Under acidic conditions, polyhistidine undergoes protonation, weakening its interaction with MCD and facilitating the release of free MCD cavities. Crucially, the PLCH micelles demonstrated a dissolution efficacy for CCs 4.50 times greater than that of free MCD alone. When combined with the STING inhibitor C-176, this strategy remarkably restored endothelial tight junctions and glycocalyx structure, alleviated chronic inflammation, and effectively suppressed atherosclerosis progression. This combined therapy successfully disrupted the detrimental cycle of atherosclerosis development, and established a virtuous intervention cycle: lipid clearance promotes inflammation inhibition, which in turn fosters endothelial repair, and restored endothelium further enhances lipid clearance. This approach provides a novel therapeutic strategy for atherosclerosis treatment. - Source: PubMed
Publication date: 2026/05/01
Zhang ShufenYu YiruLou HaiyaZheng XuetaoSong GuangtaoWang ZixuWang KaiYuan HongHu Fuqiang - Thrombospondin-1 (TSP-1) is a matricellular glycoprotein involved in the regulation of angiogenesis, immune responses, and extracellular matrix remodeling within the tumor microenvironment. Its overexpression and interaction with receptor CD47 have been associated with tumor progression and resistance to therapy. In contrast to CD47/SIRPα blockade, which is constrained by hematological and immunotoxic adverse effects, selective inhibition of the TSP-1/CD47 interaction axis may represent a mechanistically distinct and potentially safer therapeutic approach. TAX2, a 12-amino-acid cyclic peptide, was designed as an orthosteric antagonist of this interaction. Its non-clinical profile was characterized through cross-species binding assays, receptor selectivity profiling, pharmacokinetic and biodistribution analyses in rodents and dogs, in vitro off-target and cytokine release assays, and GLP-compliant toxicology studies. Human pharmacokinetics were predicted using multiple species allometric scaling. TAX2 demonstrated binding to TSP-1 from human, rodent, and canine origin, without measurable interference with CD47/SIRPα signaling under the conditions tested. The peptide exhibited rapid plasma clearance (1-4 h), dose-proportional exposure, and detectable signal in TSP-1-rich tissues and tumor-associated regions in biodistribution studies. No relevant off-target activity or unexpected immunostimulatory effects were observed. TAX2 was well tolerated at doses up to 400 mg/kg in rats and 100 mg/kg in dogs, with no hematological or systemic toxicity, and exposures exceeding the projected clinical range. Overall, these findings establish a translational non-clinical framework for TAX2 as a first-in-class TSP-1/CD47 antagonist with cross-species-reactivity and a favorable pharmacokinetic and safety profile. - Source: PubMed
Publication date: 2026/04/30
Henry AubériEtiennot MarionGhoula MariemPoli SoniaDedieu StéphaneJeanne AlbinMoniot Aurélie - Pancreatic ductal adenocarcinoma (PDAC) is characterized by a dense fibrotic stroma and aberrant tumor-associated vasculature, which impede nanoparticle (NP) penetration and accumulation, thereby reducing therapeutic efficacy. To overcome these barriers, small, selective NPs with prolonged circulation times are essential for effective tumor tissue penetration. In this study, mesoporous silica nanoparticles (MSNs) with a diameter of 45 nm were synthesized and coated with an albumin corona using a novel pH-sensitive "click" acetal linker. The albumin corona acts as a pH-responsive gatekeeper and scaffold, decorated with two distinct peptides: U11 and a CD47-derived "minimal peptide." The U11 peptide enables active targeting of PDAC cells, increasing NP uptake by 1.6- and 2.2-fold in MIA PaCa-2 and PANC-1 cells, respectively. The CD47-mimicry peptide promotes immune evasion, reducing macrophage uptake in RAW 264.7 cells by 2.3-fold compared to uncoated MSNs. The NPs were loaded with a camptothecin (CPT) gemcitabine (GEM) conjugate. The cytotoxicity of this pH-sensitive nanocarrier was evaluated in vitro against PANC-1 and MIA PaCa-2 pancreatic cancer cell lines. - Source: PubMed
Publication date: 2026/04/30
Pontón IrisNúñez SandraSemino CarlosSánchez-García David