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
- Age-related macular degeneration (AMD) is among the leading causes of blindness worldwide. Early AMD is characterized by dysfunction in the choroid, including early dropout of endothelial cells and increased deposition of the complement cascade's membrane attack complex (MAC) in the choriocapillaris. In this study, we used a single-cell RNA sequencing-based approach with barcoded antibodies to measure abundance of the MAC and other surface proteins at single cell resolution on RPE/choroid samples from four aged human donor eyes. We included antibodies to detect the MAC, CD34, CD45, and complement regulators CD55 and CD59, in addition to control antibodies. Our analysis of these data revealed cell clusters with expected gene expression profiles and antibody-based detection of CD34 and CD45 congruent with transcriptome-based cell identity. We also detected surface complement regulators CD55 and CD59 across a wide variety of cell types. Across endothelial cells, surface CD55 and CD59 appeared more abundant on venous clusters, and abundance of each was correlated with expression of a third complement regulator, clusterin (CLU). The MAC was detected on a variety of cell types, but was most abundant on the surface of cells in the macrophage family, smooth muscle cells, and pericytes. We confirmed these findings by identifying MAC deposition on choriocapillaris pericytes using immunohistochemistry for MAC, endothelial, and pericyte markers. Ultimately, these data showcase a valuable new approach to analyze gene expression and surface complement in human donor eyes, and provide novel insight into patterns of MAC deposition and complement protection in the aging human choroid. - Source: PubMed
Publication date: 2026/09/10
Jensen Renato DMullin Nathaniel KMulfaul KellyMiller Jack E BNavratil EmmaVoigt Andrew PScheetz ToddWiley Luke AStone EdwinTucker BuddMullins Robert - Corneal hyperglycemia is associated with epithelial dysfunction characterized by impaired inflammation, oxidative stress, neuropathy and innate immune mechanisms, as observed in diabetic corneal keratopathy. Therefore, the aim of the study was to investigate at cellular level the effects of moderate to severe acute and chronic challenges of glucose on human primary cultures of corneal epithelial cells (CECs). Human CECs (Innoprot, Spain) were exposed to single or repeated 15 mM or 30 mM High Glucose (HG)-supplemented media (CEC Medium containing plain 5 mM glucose), every 2 days from first stimulations and harvested at day 1 (single/acute challenge) or at days 3 and 5 (repeated/chronic challenge). Mannitol was used as osmotic control and cell sustainability were monitored by trypan blue exclusion test and MTT. Conditioned media were subjected to protein analysis while monolayers were processed for relative real-time RT-PCR. Few selected mediators belonging to the inflammatory, complement, innate receptor, oxidative, DNA enzymes and neurotrophic pathways were tested, and protein levels were assayed on selected mediators (IL-6, IL-8, CFH and C5b-9; ELISA). HG exposure induced a time- and concentration-dependent decrease in CEC metabolic activity, without a comparable reduction in cell number. Acute HG exposure promoted an inflammatory response characterized by increased , , and transcripts, together with an early modulation of complement components and increased expression of and (regulators). Chronic HG exposure induced a marked shift toward complement activation, with increased , , , and transcripts and reduced and expression, with a progressive accumulation of CFH and C5b-9 proteins in a positive relationship. Chronic HG also increased IL-6 and IL-8 protein release and induced a coordinated upregulation of , and , particularly at 30 mM HG. Antioxidant, DNA enzymes and neurotrophic pathways were differentially modulated over time, with an early response followed by chronic upregulation and reduction, progressive / expression, and a biphasic / transcriptional profile. Overall, these findings support a proposed biphasic model of the CEC response to hyperglycemia, characterized by an initial adaptive molecular response followed by progressive dysregulation under prolonged exposure. This early molecular profile might represent an adaptive response to acute metabolic stress, although further studies are required to confirm this functional protective significance. - Source: PubMed
Publication date: 2026/09/21
Dinice LuciaBalzamino Bijorn OmarEsposito GrazianaSquitti RosannaDi Zazzo AntonioMicera Alessandra - : 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