ASGR2 antibody - N-terminal region (ARP33820_P050)
- Known as:
- ASGR2 (anti-) - N-terminal region (ARP33820_P050)
- Catalog number:
- arp33820_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ASGR2 antibody - N-terminal region (ARP33820_P050)
Related genes to: ASGR2 antibody - N-terminal region (ARP33820_P050)
- Gene:
- ASGR2 NIH gene
- Name:
- asialoglycoprotein receptor 2
- Previous symbol:
- -
- Synonyms:
- CLEC4H2
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-24
- Date modifiied:
- 2016-10-05
Related products to: ASGR2 antibody - N-terminal region (ARP33820_P050)
Related articles to: ASGR2 antibody - N-terminal region (ARP33820_P050)
- In glioblastoma, the strong immunosuppression of the tumor immune microenvironment fosters tumor aggressiveness and decreases the effectiveness of therapeutic interventions, including immunotherapies. An intricate network of connections among tumor cells, stroma and infiltrating immune cells sustains immunosuppression. Lectins are immunoregulatory glycan-binding receptors contributing to immunosuppression. Their targeting is proposed as an appealing strategy for anti-cancer therapy. In this work, network-based approaches were exploited to identify a lectin profile that could dissect the complexity of tumor-immunity interactions in glioblastoma. Differential co-expression analysis, employing TCGA, CGGA and GTEx databases (145, 133 and 255 samples, respectively), identified a cluster of novel C-type lectins, with ASGR2 and CLEC12A as principal hubs. Furthermore, TIMER2.0 analysis revealed that their expression was significantly associated with immunosuppressive cells. ASGR2 and CLEC12A expression was also validated by cytofluorimetric analysis on both tumor and liquid biopsies from 20 glioblastoma patients. We report that ASGR2 and CLEC12A C-type lectins are associated with tumor-infiltrating immunosuppressive myeloid subsets and discriminate patients' poor prognosis. These results suggest that C-type lectins may contribute to the immunosuppressive network sustained by infiltrating myeloid immune cells in GB, resulting in exploitable targets for therapeutic interventions. - Source: PubMed
Publication date: 2026/03/13
Pace AngelicaAlfano CaterinaD'Angelo LucaNapoletano ChiaraZizzari Ilaria GraziaSantoro AntonioNuti MariannaFarina LorenzoPetti ManuelaRughetti Aurelia - Systemic lupus erythematosus (SLE) and idiopathic pulmonary fibrosis (IPF) share immune-inflammatory features, yet their convergent peripheral-blood transcriptomic signatures remain incompletely defined. We sought to identify shared blood gene programs linking SLE and IPF, prioritize robust cross-disease markers, and evaluate parsimonious diagnostic models with experimental and external assessments. - Source: PubMed
Publication date: 2026/02/20
Pang LijunLi YunfeiChen JunjieShang ShuangshuangLi MingHuang Chuanbing - Macrophages contribute to the immune dysregulation observed in chronic obstructive pulmonary disease (COPD). Additionally, lactylation exerts an indirect influence on COPD pathogenesis. However, the specific biomarkers linked to macrophage activation in COPD and the underlying molecular mechanisms remain poorly understood. This study aimed to identify these biomarkers and elucidate the associated molecular pathways. - Source: PubMed
Publication date: 2025/10/13
Guo HuiSun WeilinZhao FangYu YangZhao XiaoyunSun Daqiang - This study explores the link between immune cells and tuberculosis (TB) pathogenesis and progression, proposing diagnostic strategies based on immune microenvironment changes. - Source: PubMed
Publication date: 2025/07/03
Cai ZihanZhou YuyangBi ChunDing Shoupeng - Staphylococcus aureus infections are frequently complicated by metastatic foci, recurrence, and death. Antimicrobial resistance and intracellular bacterial persistence limit the effectiveness of conventional antimicrobials. Host-directed therapies could improve outcomes, but the interpretive complexity of pathogen-host interactions impedes identification of critical responses suitable for therapeutic targeting. To address this, we performed a meta-analysis of genome-scale studies aiming to prioritize host responses to S aureus. - Source: PubMed
Russell Clark DGoeldner-Thompson SeraphimaSmith EmilieMillar Jonathan EWang BoParkinson NicholasClohisey Hendry SaraSwets MaaikeFitzgerald J RossBaillie J KennethDockrell David H