CD55
- Known as:
- CD55
- Catalog number:
- 1F-230-T025
- Product Quantity:
- 25 tests
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD55
Related genes to: CD55
- Gene:
- CD55 NIH gene
- Name:
- CD55 molecule (Cromer blood group)
- Previous symbol:
- DAF
- Synonyms:
- CR, TC, CROM
- Chromosome:
- 1q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: CD55
Related articles to: CD55
- : Esophageal adenocarcinoma (EAC) is a complex disease often preceded by Barrett's esophagus. : This study aimed to identify potential drug targets and support early prevention and treatment. : We integrated -protein quantitative trait loci (-pQTLs) and genome-wide association study (GWAS) data from 35 559 individuals using Mendelian randomization to infer causal relationships, with FDR correction applied. To assess tissue relevance, the source -pQTL instruments were examined across three GTEx v8 esophageal tissues, followed by tissue-informed single-variant Wald analyses of CD55 and NDST1. Gene ontology (GO) and KEGG pathway analyses, along with protein-protein interaction (PPI) network analysis, were used to explore biological functions and interactions. Overlapping genes were identified through differential expression analysis using the GEO database. Key feature genes were screened using XGBoost and Lasso regression, and diagnostic performance was evaluated by ROC curve AUC in both training and validation sets. Immune infiltration analysis explored the tumor microenvironment, and molecular docking assessed drug potential. : We identified 28 plasma proteins causally linked to EAC. KEGG analysis revealed enrichment in oxidative stress and inflammation-related pathways. Transcriptomic validation confirmed three overlapping genes. CD55 and NDST1 emerged as key markers with strong diagnostic accuracy after Lasso and XGBoost screening. Most significant esophageal SNP-tissue associations were directionally concordant with the corresponding plasma pQTL effects, and the tissue-specific Wald estimates for CD55 and NDST1 were consistent with the primary plasma-based findings. Immune infiltration analysis showed significant changes in immune cell composition in EAC, particularly natural killer cells, plasma cells, and mast cells. Drug prediction and docking supported the druggability of these targets. : CD55 and NDST1 are promising therapeutic candidates for EAC. Drugs based on these genetic findings could improve clinical trial success rates and reduce costs. - Source: PubMed
Publication date: 2026/09/22
Zhu AijingSun HuijuanCheng CuieZhou YangHuang ShuaijingChen ZiqiHuang ShuFeng Yadong - Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal hematopoietic stem cell disorder caused by somatic mutations in the PIGA gene, resulting in loss of glycosylphosphatidylinositol (GPI)-anchored proteins, including the complement regulatory proteins, CD55 and CD59. Their absence leads to complement-mediated intravascular hemolysis. Patients may present with anemia, hemoglobinuria, renal injury, and potentially life-threatening thromboses. Complement inhibitors have transformed treatment for PNH. Terminal complement inhibitors reduce intravascular hemolysis and transfusion requirements but do not prevent C3-mediated extravascular hemolysis. Proximal complement inhibitors address both intravascular and extravascular hemolysis, but some are associated with a higher risk of breakthrough hemolysis (BTH). This article describes a transfusion-independent PNH patient on pegcetacoplan who developed severe BTH post-HLA desensitization using therapeutic plasma exchange (PLE) prior to hematopoietic cell transplantation. - Source: PubMed
Publication date: 2026/09/17
Raman GaneshVivek MeghanaHasan RidaKeel SiobánConnelly-Smith Laura - Local expression of complement components in the kidney has been reported sporadically in both diseased and normal kidneys. This study aimed to comprehensively characterize the expression of complement components in human glomerular mesangial cells (GMCs), glomerular endothelial cells (GECs), podocytes, and proximal tubular epithelial cells (PTECs) in non-diseased renal tissue. - Source: PubMed
Publication date: 2026/09/01
Gao YuemingLi QiWang YueDeng Zhenling - Evidence-based, mechanism-guided therapies are urgently needed for treating monogenic inflammatory bowel disease (mIBD). For such rare diseases, mechanistic insight is essential to guide treatment when conventional clinical trials are often not feasible. We aimed to summarize literature-based evidence and to identify knowledge gaps. - Source: PubMed
Yeh Pai-JuiCharlesworth James E GTaylor HenryAshton James JNash KatrinaLam Kin Hangde Ridder LissyVuijk Stephanie AYe ZiqingHuang YingBildstein TaniaHaller WolframJones Kelsey D JShouval Dror SWeiss BatiaLau Yu LungBui-Thi-Thuy QuynhMuise Aleixo MRichards DuncanTravis SimonTurner DanUhlig Holm H - Epidermal growth factor receptor (EGFR) mutations represent a central oncogenic driver in non-small cell lung cancer (NSCLC). While EGFR tyrosine kinase inhibitors (TKIs) have revolutionized the management of NSCLC, acquired resistance remains a major hurdle. In response, antibody-based therapeutic strategies have gained increasing attention as a means to overcome TKI resistance and extend disease control. This review synthesizes the rapidly evolving landscape of antibody-based therapeutics for EGFR-mutant NSCLC. We first summarize the mechanisms of monoclonal antibodies directly targeting EGFR, including cetuximab and necitumumab, and discuss their therapeutic limitations. We then highlight the emergence of bispecific antibodies designed to simultaneously target EGFR and key resistance pathways, such as MET. In addition, we review combination strategies integrating EGFR inhibition with antibodies directed against alternative oncogenic pathways or the tumor microenvironment, including anti-angiogenic agents such as bevacizumab. A major focus of this review is antibody-drug conjugates (ADCs) targeting novel surface antigens, including HER2, HER3, and TROP2. By delivering highly potent cytotoxic payloads selectively to tumor cells, these ADCs have demonstrated remarkable clinical efficacy in EGFR TKI-resistant settings. Furthermore, we examine the complex and evolving role of immunotherapy in EGFR-mutant NSCLC. Beyond immune checkpoint blockade, we discuss emerging immunomodulatory strategies targeting the adenosine pathway (CD73), phagocytosis checkpoints (CD24), and complement regulatory proteins (CD55/CD59). Finally, we explore advanced antibody modalities, including immune-engaging bispecific antibodies and next-generation ADCs. Collectively, antibody-based therapies are reshaping the treatment landscape through diverse mechanisms, offering renewed promise for overcoming resistance and improving outcomes in EGFR-mutant NSCLC. - Source: PubMed
Publication date: 2026/09/11
Chen XinranLiang JiaqiZhu JunkanHuang XiaolongHu YiduLin ZongwuZhan Cheng