ArticleOncotarget2016
CD93 and dystroglycan cooperation in human endothelial cell adhesion and migration adhesion and migration.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 63 citations in OpenAlex.
- Rational design of hammerhead ribozymes as CD93 silencing tools for vascular diseases.Molecular therapy. Nucleic acids · 2026Article
- Serum CD93 as a Potential Diagnostic Biomarker for Endometrial Cancer: A Case-Control Study.Journal of clinical medicine · 2026Article
- Endothelial cell senescence shapes T cell activity in late-stage of chronic obstructive pulmonary disease.Cell death discovery · 2026Article
- Multi-omics analysis reveals metabolic diversity underlying endothelial cell functions.Life science alliance · 2026Article
- Endothelial cell-released CD93 contributes to podocyte injury in idiopathic nephrotic syndrome.Science translational medicine · 2026Article
- CD93 in Health and Disease: Bridging Physiological Functions and Clinical Applications.International journal of molecular sciences · 2025Review
- Dynamics of T Cell-Mediated Immune Signaling Network During Pathogenesis of Chronic Obstructive Pulmonary Disease.Yonsei medical journal · 2025Article
- CD93: A Promising NETs-Related Biomarker for Diagnosis and Therapy in Actinic Keratosis.OncoTargets and therapy · 2025Article
- Immuno-PET Imaging of CD93 Expression withMolecular pharmaceutics · 2024Article
- Genome-wide study identifies novel genes associated with bone toxicities in children with acute lymphoblastic leukaemia.British journal of haematology · 2024Article
- IGFBP7 mediates oxLDL-induced human vascular endothelial cell injury by suppressing the expression of SIRT1.Heliyon · 2024Article
- Group XIV C-type lectins: emerging targets in tumor angiogenesis.Angiogenesis · 2024Review
- Structural insight into CD93 recognition by IGFBP7.Structure (London, England : 1993) · 2024Article
- Article
- Angiogenesis modulated by CD93 and its natural ligands IGFBP7 and MMRN2: a new target to facilitate solid tumor therapy by vasculature normalization.Cancer cell international · 2023Review
- Role of CD93 in Health and Disease.Cells · 2023Review
- CD93 overexpresses in liver hepatocellular carcinoma and represents a potential immunotherapy target.Frontiers in immunology · 2023Article
- CD93 is Associated with Glioma-related Malignant Processes and Immunosuppressive Cell Infiltration as an Inspiring Biomarker of Survivance.Journal of molecular neuroscience : MN · 2022Article
- A glimpse into the past: phylogenesis and protein domain analysis of the group XIV of C-type lectins in vertebrates.BMC genomics · 2022Article
- Bioinformatics Approaches to Predict Mutation Effects in the Binding Site of the Proangiogenic Molecule CD93.Frontiers in bioinformatics · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD93 is a transmembrane glycoprotein predominantly expressed in endothelial cells. Although CD93 displays proangiogenic activity, its molecular function in angiogenesis still needs to be clarified. To get molecular insight into the biological role of CD93 in the endothelium, we performed proteomic analyses to examine changes in the protein profile of endothelial cells after CD93 silencing. Among differentially expressed proteins, we identified dystroglycan, a laminin-binding protein involved in angiogenesis, whose expression is increased in vascular endothelial cells within malignant tumors. Using immunofluorescence, FRET, and proximity ligation analyses, we observed a close interaction between CD93 and β-dystroglycan. Moreover, silencing experiments showed that CD93 and dystroglycan promoted endothelial cell migration and organization into capillary-like structures. CD93 proved to be phosphorylated on tyrosine 628 and 644 following cell adhesion on laminin through dystroglycan. This phosphorylation was shown to be necessary for a proper endothelial migratory phenotype. Moreover, we showed that during cell spreading phosphorylated CD93 recruited the signaling protein Cbl, which in turn was phosphorylated on tyrosine 774. Altogether, our results identify a new signaling pathway which is activated by the cooperation between CD93 and dystroglycan and involved in the control of endothelial cell function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.