CD50
- Known as:
- CD50
- Catalog number:
- 10-452-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD50
Related genes to: CD50
- Gene:
- ICAM3 NIH gene
- Name:
- intercellular adhesion molecule 3
- Previous symbol:
- -
- Synonyms:
- CDW50, ICAM-R, CD50
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-19
- Date modifiied:
- 2016-01-15
Related products to: CD50
Anti-CD50 (azide-free) AntibodyAnti-CD50 azide-free antibodyAntibodies: Mouse Monoclonal to CD50 _ ICAM-3, Species Reactivity: Human, Clone: MEM-04, Isotype: IgG1Antibodies: Mouse Monoclonal to CD50 _ ICAM-3, Species Reactivity: Human, Clone: MEM-04, Isotype: IgG1Antibodies: Mouse Monoclonal to CD50 _ ICAM-3, Species Reactivity: Human, Clone: MEM-171, Isotype: IgG1Antibodies: Mouse Monoclonal to CD50 _ ICAM-3, Species Reactivity: Human, Clone: MEM-171, Isotype: IgG1Antibodies: Mouse Monoclonal to CD50 _ ICAM-3, Species Reactivity: Human, Clone: MEM-171, Isotype: IgG1Antibodies: Mouse Monoclonal to CD50 _ ICAM-3, Species Reactivity: Human, Clone: MEM-171, Isotype: IgG1Antibodies: Mouse Monoclonal to CD50 _ ICAM-3, Species Reactivity: Human, Clone: MEM-171, Isotype: IgG1Antibodies: Mouse Monoclonal to CD50 _ ICAM-3, Species Reactivity: Human, Clone: MEM-171, Isotype: IgG1Antibodies: Mouse Monoclonal to CD50 _ ICAM-3, Species Reactivity: Human, Clone: MEM-171, Isotype: IgG1Antibodies: Mouse Monoclonal to CD50 _ ICAM-3, Species Reactivity: Human, Clone: MEM-171, Isotype: IgG1Anti_Human, mab CD50 Source Mouseanti_ICAM_3, Leukocytes Recognition human CD50 antigen Clone ICO_60anti_ICAM_3, Leukocytes Recognition human CD50 antigen Clone ICO_60 Related articles to: CD50
- : Brain metastasis is associated with poor prognosis in lung adenocarcinoma (LUAD). Anoikis resistance may contribute to tumor cell survival during metastatic dissemination and brain colonization; however, robust biomarkers for prognostic stratification and brain metastasis-associated classification remain limited. This study aimed to investigate anoikis-related molecular features in LUAD brain metastasis and develop a machine learning-based signature for prognostic assessment and exploratory classification of primary and brain-metastatic LUAD samples. : We integrated single-cell and multi-cohort bulk transcriptomic data. Single-cell analysis was performed to characterize anoikis-related cellular states and intercellular communication in primary and brain-metastatic LUAD samples. In the bulk transcriptomic analysis, TCGA-LUAD was used for prognostic feature selection and risk-model construction, and GSE26939 was used for external prognostic validation. The classification performance of the fixed signature for distinguishing primary LUAD from brain-metastatic LUAD samples was further evaluated in GSE161116 and GSE271259. Immune microenvironment features were assessed, and an LLM-assisted exploratory drug-screening strategy combined with molecular docking was used to prioritize candidate compounds. : Single-cell analysis suggested that metastatic epithelial cells exhibited enhanced anoikis-related activity, accompanied by macrophage-associated SPP1-CD44 and MIF-(CD74+CXCR4) communication patterns. Machine learning-based feature selection identified an eight-gene signature consisting of , , , , , , , and . The signature showed prognostic value in TCGA-LUAD and GSE26939 and demonstrated exploratory classification performance in distinguishing primary LUAD from brain-metastatic LUAD samples. High-risk patients exhibited immune microenvironment alterations and enrichment of tumor progression-related pathways. LLM-assisted compound prioritization and molecular docking highlighted resveratrol and SB431542 as hypothesis-generating candidates with predicted interactions with core targets. : This study identified an anoikis-related eight-gene signature for LUAD prognostic stratification and exploratory brain metastasis-associated classification. The findings suggest the potential involvement of anoikis-related tumor-microenvironment interactions in LUAD brain metastasis and provide candidate genes and compounds for further experimental validation. - Source: PubMed
Publication date: 2026/06/17
Wu JunhongZhang BaijunLiu Hengrui - Carotid plaque is an early manifestation of atherosclerosis and is closely associated with the risk of myocardial ischaemia, ischaemic stroke and other atherosclerotic cardiovascular diseases (ASCVDs). To identify new protein biomarkers associated with carotid plaque, which will enhance early warning of ASCVDs DESIGN: Nested case-control study within a prospective cohort, with external assessment of transportability in an independent population-based cohort. - Source: PubMed
Publication date: 2026/06/25
Jin BolinLin ChunyingWu ChaoqunChen BowangHan YiZhang XiaoyanBai XuekeYang YangCui JianlanXu WeiSong LijuanYang HaoHe WenyanZhang YanGao YanLi Xi - Pediatric sepsis is increasingly recognized as a syndrome involving immune-vascular dysregulation. However, most pediatric biomarker studies focus on individual molecules rather than coordinated patterns of leukocyte-endothelial activation. This study aimed to evaluate whether children diagnosed with sepsis within 48 h of admission showed a coordinated soluble adhesion-molecule activation profile measured at enrollment. This prospective cohort study included 144 children aged 1-60 months with suspected infection enrolled at Dong Nai Children's Hospital, Vietnam, from May 2021 to October 2022. Blood samples were collected at enrollment. Sepsis was classified according to the 2005 International Pediatric Sepsis Consensus Conference (IPSCC) criteria within 48 h of admission. Twelve soluble adhesion molecules were measured using a multiplex immunoassay. A composite adhesion activation score was derived by log2 transformation, z-score standardization, and averaging across the 12 markers. Principal component analysis (PCA) was used as an exploratory method to summarize the shared variation across the adhesion-molecule panel. C-reactive protein (CRP) was included as a routinely available inflammatory comparator. Among 144 children, 32 (22.2%) were diagnosed with sepsis within 48 h of admission. Individual marker discrimination was strongest for L-selectin (area under the receiver operating characteristic curve [AUC] 0.883), followed by soluble vascular cell adhesion molecule-1 (sVCAM-1; AUC 0.855), intercellular adhesion molecule-3 (ICAM-3; AUC 0.838), P-selectin glycoprotein ligand-1 (PSGL-1; AUC 0.836), E-selectin (AUC 0.819), and intercellular adhesion molecule-2 (ICAM-2; AUC 0.819). CRP also differed between children with and without sepsis but had a lower AUC than the leading adhesion molecules in descriptive ROC analyses. The composite adhesion activation score was strongly associated with sepsis (odds ratio 7.95 per 1-standard deviation increase; 95% confidence interval 3.44-18.40; < 0.001) and showed good discrimination (AUC 0.855; 95% confidence interval 0.776-0.931). The first principal component explained 70.0% of biomarker variance, consistent with coordinated elevation of correlated adhesion molecules. In this prospective Vietnamese pediatric cohort, children diagnosed with sepsis within 48 h of admission showed coordinated elevation of soluble adhesion molecules measured at enrollment. These findings support the biological relevance of leukocyte-endothelial activation in pediatric sepsis. However, the adhesion-molecule activation profile should be considered exploratory and hypothesis-generating, requiring external validation and further evaluation against simplified, clinically feasible biomarker approaches. - Source: PubMed
Publication date: 2026/06/09
Liem Bui ThanhThien Chu VanNghia Nguyen TrongPhong Le AnhDinh Ngo NhuLuan Nguyen HuyNguyen Phung Nguyen The - Severe eosinophilic asthma (SEA) is driven by type 2 (T2) inflammation, characterised by dysregulated cytokine release and aberrant expression of adhesion molecules involved in immune cell trafficking and activation. Despite the established role of intercellular adhesion molecules (ICAMs) and L-selectin (CD62L) in these processes, their dysregulation in SEA and their potential remodulation in response to biologic therapy remain unclear.To investigate the expression of adhesion molecules (ICAM-1, ICAM-3, CD62L) on T-cell subsets in SEA, their modulation by IL-25 and IL-33, and the immunological impact of benralizumab therapy. - Source: PubMed
Publication date: 2026/03/16
Bergantini LauraPaggi IrenePianigiani TommasoBiancucci Sarad'Alessandro MirianaBargagli ElenaCameli Paolo - It is well established that the function of DCs (dendritic cells) is impaired during malaria infection; however, the underlying mechanisms responsible for this impairment remain poorly understood. In this study, we found that ATG5 (autophagy related 5) deficiency in DCs significantly suppressed the growth of malaria blood-stage parasites, and this effect was independent of both canonical and non-canonical macroautophagy/autophagy pathways in these cells. The reduced parasite growth observed in mice was associated with an enhanced parasite-specific CD4 T cell response, which provided crucial support for the functional activation of Plasmodium-specific CD8 T cells. Mechanistically, ATG5 deficiency led to a marked increase in the expression of the phagocytic receptor CD209A/DC-SIGN on conventional DCs (cDCs), thereby enhancing their capacity to activate Plasmodium-specific CD4 T cell responses. Furthermore, the expression of CD209A was mediated by the TLR2 (toll-like receptor 2) signaling pathway, which was significantly augmented in the absence of ATG5. Thus, we reveal a novel role for ATG5 in modulating anti-malarial cellular immune responses by influencing TLR2-mediated CD209A expression in cDCs. These findings not only enhance our understanding of impaired DC function during malaria infection but also provide valuable insights for the design of more effective malaria vaccines. ATG5: autophagy related 5; cDCs: conventional dendritic cells; CFSE: carboxyfluorescein succinimidyl ester; DC-SIGN: dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin; IFNG/IFN-γ: interferon gamma; LAP: LC3-associated phagocytosis; MAPK: mitogen-activated protein kinase; NFKB1/NF-κB: nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105; pRBCs: parasitized red blood cells; PRRs: pattern recognition receptors; TLR2: toll-like receptor 2; TNF/TNF-α: tumor necrosis factor. - Source: PubMed
Publication date: 2026/05/29
Fan YonglingJiao ShimingLi HangyuGao YuanliFang JiaqinZhang KunGuo ShuaiXu WenyueLiu Taiping