Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
| Cat.No. | Product Name | Price |
|---|---|---|
| CSC-DC002782 | Panoply™ Human CD93 Knockdown Stable Cell Line | Inquiry |
| CSC-SC002782 | Panoply™ Human CD93 Over-expressing Stable Cell Line | Inquiry |
| CLOE-0601 | Human CD93(His) HEK293 Cell Lysate | Inquiry |
| CLOE-0604 | Human CD93(Fc) HEK293 Cell Lysate | Inquiry |
| CLOE-2063 | Rat Cd93 (His) HEK293 Cell Lysate | Inquiry |
| CSC-RO0858 | Human CD93 Stable Cell Line - CHO-K1 | Inquiry |
| CSC-RO0862 | Mouse Cd93 Stable Cell Line - HEK293T | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| AD03379Z | Human CD93 adenoviral particles | Inquiry |
| LV08492L | human CD93 (NM_012072) lentivirus particles | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| SHG159865 | shRNA set against Mouse Cd93(NM_010740.3) | Inquiry |
| SHG160045 | shRNA set against Human CD93(NM_012072.3) | Inquiry |
| SHH259494 | shRNA set against Mouse CD93 (NM_010740.3) | Inquiry |
| SHH259497 | shRNA set against Rat CD93 (NM_053383.1) | Inquiry |
| SHW003260 | shRNA set against Chicken CD93 (NM_001199451) | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| CDFL002472 | Mouse Cd93 cDNA Clone(NM_010740.3) | Inquiry |
| CDFR013132 | Rat Cd93 cDNA Clone(NM_053383.1) | Inquiry |
| MiUTR1H-01916 | CD93 miRNA 3'UTR clone | Inquiry |
| MiUTR1M-02806 | CD93 miRNA 3'UTR clone | Inquiry |
| MiUTR1R-00641 | CD93 miRNA 3'UTR clone | Inquiry |
| CDCB164735 | Chicken CD93 ORF Clone (NM_001199451) | Inquiry |
| CDCB186591 | Rabbit CD93 ORF clone (XM_002710939.2) | Inquiry |
| CDCL183442 | Mouse CD93 ORF clone(NM_010740.3) | Inquiry |
| CDCL183443 | Rat CD93 ORF clone(NM_053383.1) | Inquiry |
| CDCR295332 | Human CD93 ORF Clone(NM_012072.3) | Inquiry |
| CDCS413184 | Human CD93 ORF Clone (BC028075) | Inquiry |
The CD93 gene, located on human chromosome 20p11.21, encodes a type I transmembrane glycoprotein. Initially identified as a myeloid cell-specific surface marker and proposed as a receptor for complement component C1q (hence the name C1qRp), subsequent studies have redefined its role primarily in cell adhesion and clearance of apoptotic cells.
Structurally, CD93 possesses a distinctive extracellular region comprising a C-type lectin-like domain, multiple EGF-like repeats, and a heavily glycosylated mucin-like domain, suggesting its involvement in protein–protein and protein–carbohydrate interactions. Its relatively short intracellular domain interacts with moesin, a member of the ERM (ezrin-radixin-moesin) family, which links membrane proteins to the actin cytoskeleton, providing structural support for cell morphology and motility. CD93 expression is not limited to myeloid cells; it is highly expressed on endothelial cells, particularly activated and proliferating vascular endothelium, highlighting its potential importance in vascular biology.
CD93 exhibits multifaceted biological functions, primarily centered on innate immune regulation and angiogenesis. In the immune system, CD93 acts as a functional receptor for opsonins including C1q, mannose-binding lectin, and surfactant protein A. These molecules mark apoptotic cells or immune complexes, and CD93 recognition enhances phagocytic uptake by macrophages and other phagocytes, promoting efficient clearance of apoptotic cells. This process is crucial for homeostasis, preventing release of intracellular toxins and autoimmune activation.
Figure 1. The CD93 signaling pathway in migrating endothelial cells. (Barbera S, et al., 2021)
In vascular biology, CD93 is a marker of endothelial activation and actively promotes angiogenesis. Mechanistically, CD93 interacts with β-dystroglycan, recruiting and activating SRC kinase, leading to CBL adaptor phosphorylation and formation of docking platforms for downstream molecules such as CRKL, ultimately driving endothelial cell migration, a key step in neovascularization. Recent studies also identified CD93 as the endothelial receptor for extracellular matrix glycoproteins multimerin-2 (MMRN2) and IGFBP7, which regulate cell adhesion, spreading, and tubular structure formation. Furthermore, CD93 modulates VEGFR2 signaling, influencing endothelial barrier integrity. Collectively, CD93 functions as a cell-surface integrator, coordinating extracellular matrix signals with cytoskeletal rearrangements to regulate immune clearance and tissue remodeling.
CD93's clinical relevance is increasingly recognized, particularly as a biomarker and therapeutic target in vascular diseases and oncology. In tumors, CD93 plays a central role in tumor angiogenesis, making it an attractive anti-angiogenic target. Elevated CD93 expression on endothelial cells is observed in glioblastoma, colorectal cancer, and lung cancer, often correlating with poor prognosis. Preclinical studies show that monoclonal antibody blockade or gene silencing of CD93 inhibits tumor vascularization, causing tumor necrosis and growth restriction, supporting its potential as a therapeutic target. Given resistance issues with VEGF-targeted therapies, CD93-targeted interventions offer a promising complementary or alternative angiogenesis strategy.
Beyond oncology, CD93 may contribute to pathological angiogenesis in conditions such as atherosclerosis and diabetic retinopathy. Its role in apoptotic cell clearance also suggests potential links to autoimmune diseases like systemic lupus erythematosus, where defective clearance triggers autoimmune activation. While no CD93-targeted therapies have yet entered clinical use, ongoing studies exploring its interaction with MMRN2 and IGFBP7 may enable future interventions for abnormal angiogenesis or immune dysregulation. Additionally, soluble CD93 levels in serum are being investigated as a biomarker of endothelial activation and inflammatory disease activity. Overall, CD93 represents a multifunctional interface between innate immunity and vascular biology, with emerging diagnostic and therapeutic potential across multiple human diseases.
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