Affinage

CD93

Complement component C1q receptor · UniProt Q9NPY3

Length
652 aa
Mass
68.6 kDa
Annotated
2026-06-09
63 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CD93 (C1qR(P)/C1qRP) is a myeloid- and endothelial-restricted type I transmembrane protein, built from an N-terminal C-type carbohydrate-recognition domain and five EGF-like repeats, that functions as a phagocytic receptor coupling the recognition of defense collagens to enhanced clearance of particles and apoptotic cells (PMID:9047234, PMID:9469455). It is the receptor through which the structurally related ligands C1q, mannose-binding lectin, and surfactant protein A enhance FcR- and CR1-mediated phagocytosis, recognition occurring through a GE(K/Q/R)GEP motif in the collagen-like domain of these ligands (PMID:9047234, PMID:11533031, PMID:11390503). Signal transduction depends strictly on the short cytoplasmic tail: blocking or cross-linking this domain modulates phagocytic enhancement (PMID:10648005, PMID:11074255), and direct mAb ligation alone drives a pro-phagocytic signal (PMID:10092817). The tail engages the ERM protein moesin through juxtamembrane positively charged residues, tying the receptor to the cytoskeleton, and the C-terminal class I PDZ-binding motif recruits the adaptor GIPC, a peptide of which enhances monocyte phagocytosis (PMID:15459234, PMID:15819698). CD93 is heavily O-glycosylated, and this glycosylation is required for its molecular weight and for stable retention at the cell surface, without which the protein is shed or degraded (PMID:10092817, PMID:12891708). In endothelial cells, C1q-bearing immune complexes or anti-CD93 cross-linking drive IL-8 secretion via PTK- and MAPK-dependent signaling (PMID:11531942). CD93-deficient mice establish an in vivo requirement for CD93 in apoptotic cell clearance, but not in complement- or FcγR-dependent phagocytosis enhancement (PMID:15004139). The ectodomain is released by a metalloproteinase distinct from ADAM17 upon inflammatory stimulation, generating soluble CD93 in plasma (PMID:16002728). Beyond its phagocytic role, CD93 regulates tumor vasculature, where its blockade upregulates ICAM1/VCAM1, matures vessels, and enhances T-cell infiltration (PMID:39805660), and in pleural mesothelial cells it suppresses CCL21 secretion to dampen anti-tumor immunity (PMID:38250037).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 1994 High

    Before its molecular identity was known, the question was whether a single defined surface receptor accounted for C1q-enhanced phagocytosis; defining a 126 kDa protein recognized by inhibitory mAbs separated this receptor from the C1q superoxide-triggering receptor.

    Evidence Immunoprecipitation, functional phagocytosis and radioligand binding inhibition with three mAbs on phagocytic cells

    PMID:8144968

    Open questions at the time
    • Receptor cDNA and domain structure not yet defined
    • CD43 co-IP raised but multi-subunit composition unresolved
  2. 1997 High

    The molecular nature of the phagocytic C1q receptor was unknown; cloning revealed a type I transmembrane protein with a C-type CRD and EGF repeats that mediates enhancement triggered by three related defense collagens.

    Evidence mAb affinity purification, amino acid sequencing, cDNA cloning, and functional inhibition across C1q/MBL/SPA

    PMID:9047234

    Open questions at the time
    • Cytoplasmic signaling partners unidentified
    • Endogenous ligand-binding surface on the receptor not mapped
  3. 1999 High

    It was unclear how the receptor reconciled its predicted versus observed mass and whether ligand binding was required for signaling; O-glycosylation was shown to account for the mass and mAb ligation alone shown to drive phagocytosis.

    Evidence CHO transfection, glycosidase and inhibitor treatment, in vitro translation, mAb cross-linking phagocytosis assay

    PMID:10092817

    Open questions at the time
    • Downstream signaling cascade not defined
    • Site of functionally critical O-glycans not mapped
  4. 2001 High

    The ligand determinant driving CD93-mediated phagocytosis was unknown; a GE(K/Q/R)GEP motif in the collagen-like domain of defense collagens was identified as required for the enhancement signal.

    Evidence Site-directed mutagenesis of recombinant MBL and monocyte phagocytosis assays

    PMID:11533031

    Open questions at the time
    • Direct binding of this motif to the CD93 ectodomain not demonstrated
    • Whether C1q and SPA use the identical motif geometry not resolved
  5. 2003 High

    The functional consequence of CD93 O-glycosylation was undefined; glycosylation was shown to stabilize surface retention, with unglycosylated protein released or degraded.

    Evidence Glycosylation inhibitor and ldlD glycosylation-deficient cells with metabolic labeling and surface expression analysis

    PMID:12891708

    Open questions at the time
    • Mechanism of glycosylation-dependent retention vs. shedding not resolved
    • Link to the inflammatory metalloproteinase shedding pathway not established
  6. 2005 High

    How the cytoplasmic tail couples to intracellular machinery was unknown; the tail was shown to bind moesin (cytoskeletal coupling) and GIPC (PDZ adaptor), with a tail peptide enhancing phagocytosis.

    Evidence Yeast two-hybrid, GST pulldown with lysate and recombinant moesin, co-capping, deletion mutagenesis, cell-permeable peptide assays

    PMID:15459234 PMID:15819698

    Open questions at the time
    • Order and interdependence of moesin vs. GIPC binding not resolved
    • Downstream effectors of GIPC recruitment unidentified
  7. 2005 High

    Whether CD93 levels are dynamically regulated at the surface was open; inflammatory stimuli were shown to trigger metalloproteinase-dependent (ADAM17-independent) ectodomain shedding generating plasma soluble CD93.

    Evidence Flow cytometry, ELISA of shed ectodomain and plasma sCD93, metalloproteinase inhibitor and ADAM17-deficient conditions

    PMID:16002728

    Open questions at the time
    • Identity of the responsible metalloproteinase unknown
    • Function of soluble CD93 not defined
  8. 2004 High

    The in vivo physiological role was untested; CD93-knockout mice revealed a requirement in apoptotic cell clearance but not in complement/FcγR phagocytosis enhancement, decoupling the in vitro and in vivo functions.

    Evidence CD93 knockout mice, in vivo apoptotic cell clearance, in vitro phagocytosis, intravital microscopy

    PMID:15004139

    Open questions at the time
    • Bridging ligand/molecular mechanism for apoptotic cell clearance unidentified
    • Reconciliation with mAb-based phagocytosis data not achieved
  9. 2001 Medium

    Whether CD93 signals in non-phagocytic lineages was unclear; in endothelial cells C1q immune complexes and anti-CD93 cross-linking were shown to induce IL-8 via PTK/MAPK pathways.

    Evidence HUVEC stimulation, mAb cross-linking, genistein and UO126 inhibitors, IL-8 mRNA and protein assays

    PMID:11531942

    Open questions at the time
    • Proximal kinases linking CD93 to MAPK not identified
    • Whether endothelial signaling uses the same tail partners as myeloid cells unknown
  10. 2002 Medium

    Beyond differentiated myeloid/endothelial cells, CD93 was found to mark a rare repopulating stem cell population with hematopoietic and hepatic differentiation potential.

    Evidence FACS purification and NOD/SCID xenograft transplantation

    PMID:12140365

    Open questions at the time
    • Functional role of CD93 in stemness not tested
    • Mechanism of hepatic differentiation potential undefined
  11. 2025 Medium

    The role of CD93 on tumor vasculature was undefined; blockade was shown to upregulate ICAM1/VCAM1, mature vessels, and enhance effector T-cell infiltration, identifying CD93 as a regulator of vascular immune exclusion.

    Evidence Anti-CD93 antibody treatment in mouse melanoma, vascular and TIL profiling, ICAM1/VCAM1 neutralization, adoptive T-cell transfer

    PMID:38250037 PMID:39805660

    Open questions at the time
    • Ligand/signaling axis driving adhesion molecule suppression unresolved
    • Pleural mesothelial CCL21 suppression mechanism downstream of CD93 not fully defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • The molecular basis by which CD93 recognizes apoptotic cells in vivo and the proximal signaling that converts ligand engagement into phagocytic, IL-8, and vascular outputs remain unresolved.
  • No defined apoptotic-cell bridging ligand or direct binding partner on the ectodomain
  • Proximal kinase/effector linking the cytoplasmic tail to MAPK and cytoskeletal remodeling unidentified
  • Identity of the shedding metalloproteinase and function of soluble CD93 unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0038024 cargo receptor activity 3 GO:0060089 molecular transducer activity 2 GO:0008092 cytoskeletal protein binding 1 GO:0060090 molecular adaptor activity 1
Localization
GO:0005886 plasma membrane 3 GO:0031410 cytoplasmic vesicle 2 GO:0005576 extracellular region 1
Pathway
R-HSA-168256 Immune System 3 R-HSA-5653656 Vesicle-mediated transport 3 R-HSA-162582 Signal Transduction 2
Partners
C1QACD43GIPC1MBL2MSNSFTPA1

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 CD93 (C1qR(P)) was identified as a novel type I transmembrane protein with a C-type carbohydrate recognition domain, five EGF-like domains, a transmembrane domain, and a short cytoplasmic tail. Monoclonal antibodies R3 and R139, which inhibit C1q/MBL/SPA-mediated enhancement of phagocytosis, were used to purify the protein and clone its cDNA, establishing it as the receptor mediating enhanced phagocytosis triggered by these three structurally related ligands. Protein purification via mAb affinity, amino acid sequencing, cDNA cloning, anti-peptide antiserum generation, functional inhibition assays Immunity High 9047234
1999 CD93 (C1qRP) is heavily O-glycosylated, and this O-linked glycosylation is required for proper molecular weight and cell surface expression. Direct cross-linking of CD93 by immobilized anti-CD93 mAb R3 triggers enhanced phagocytic capacity in the absence of ligand, demonstrating that CD93 ligation directly transduces a pro-phagocytic signal. The protein backbone alone (without glycosylation) migrates at the predicted molecular weight; extensive O-glycosylation accounts for the discrepancy between predicted and observed molecular weight. CHO cell transfection, glycosylation inhibitors, glycosidase cleavage, in vitro translation, functional phagocytosis assay with mAb cross-linking Journal of immunology High 10092817
2003 O-glycosylation stabilizes CD93 at the cell surface. When O-glycosylation is inhibited (by BAG in U937 cells or by reversible glycosylation defect in ldlD CHO cells), CD93 is synthesized but rapidly released into culture supernatant or degraded rather than being retained at the plasma membrane. Glycosylation inhibitor treatment, glycosylation-deficient cell line (ldlD), metabolic labeling, cell surface expression analysis Journal of cellular physiology High 12891708
2004 CD93 cytoplasmic tail interacts with GIPC, a PDZ domain-containing adaptor protein. The interaction requires a class I PDZ-binding domain in the CD93 C-terminus and four positively charged juxtamembrane amino acids. A cell-permeable peptide encoding the C-terminal 11 amino acids of CD93 enhanced phagocytosis in human monocytes, linking this intracellular protein-protein interaction to modulation of phagocytic activity. Yeast two-hybrid screen, GST fusion protein pulldown assay, cell-permeable peptide functional assay in human monocytes Journal of leukocyte biology High 15459234
2005 The ERM protein moesin binds to the CD93 cytoplasmic tail via the first four positively charged amino acids in the juxtamembrane region. Moesin co-caps with CD93 in intact human monocytes. Deletion of the last 11 C-terminal amino acids of CD93 dramatically increases moesin binding in cell lysate assays but not with purified recombinant moesin, suggesting that other intracellular molecules compete for or regulate this interaction. PIP2 enhances moesin binding to the CD93 cytoplasmic domain. GST fusion protein binding assay with cell lysates and recombinant moesin, co-capping in human monocytes, deletion mutagenesis, PIP2 addition experiments Immunology High 15819698
2004 CD93-deficient mice show a significant defect in clearance of apoptotic cells in vivo (human Jurkat T cells and murine thymocytes), but not in complement- or FcγR-dependent phagocytosis in vitro or in vivo. CD93-deficient macrophages plated on C1q-coated surfaces showed normal enhancement of complement- and FcγR-dependent RBC uptake. No supporting role was found for CD93 as an adhesion molecule in leukocyte recruitment assessed by intravital microscopy. CD93 knockout mice, in vivo apoptotic cell clearance assay, in vitro phagocytosis assays, intravital microscopy, peritoneal cell recruitment assays Journal of immunology High 15004139
2005 CD93 undergoes ectodomain shedding from the surface of human monocytes and neutrophils. Shedding is induced by phorbol dibutyrate, TNF-α, LPS, and CD93 cross-linking with immobilized anti-CD93 mAbs. The shed ectodomain retains the N-terminal CRD and EGF repeats. Shedding is inhibited by metalloproteinase inhibitor 1,10-phenanthroline but is independent of ADAM17 (TACE). A soluble form of CD93 is detected in human plasma. Neutrophil surface CD93 lost by shedding is replaced from intracellular stores. Flow cytometry, ELISA detection of shed ectodomain and plasma sCD93, metalloproteinase inhibitor treatment, immunoblotting for intracellular domain-containing cleavage products, ADAM17-deficient conditions Journal of immunology High 16002728
2000 Neonatal rat microglia express C1qR(P)/CD93, as assessed by flow cytometry and immunocytochemistry. Substrate-bound C1q enhances both FcR- and CR1-mediated phagocytosis two- to fourfold in microglia. Introduction of an antibody against the cytoplasmic C-terminal domain of CD93 into microglia by electroporation markedly diminished C1q-enhanced phagocytosis, indicating that the cytoplasmic domain of CD93 is required to transduce the phagocytic enhancement signal. Flow cytometry, immunocytochemistry, phagocytosis assay, intracellular antibody delivery by electroporation Journal of leukocyte biology Medium 10648005
2001 C1qR(P)/CD93 on microglia mediates C1q-enhanced phagocytosis of antibody-opsonized amyloid-β immune complexes. Mannose binding lectin and lung surfactant protein A, other ligands of C1qR(P), also enhanced microglial ingestion of suboptimally opsonized IgG-fAβ complexes, whereas control proteins did not, demonstrating ligand specificity through CD93. Microglial phagocytosis assay with C1q, MBL, SPA ligands; antibody blocking experiments Journal of immunology Medium 11390503
2001 C1q-bearing immune complexes (but not monomeric C1q) induce IL-8 secretion in human umbilical vein endothelial cells via protein tyrosine kinase (PTK)- and MAPK-dependent pathways. The cross-linking anti-CD93 mAb R3 (against the 126 kDa phagocytic C1qR) also stimulated IL-8 production, indicating CD93 transduces this signal. IL-8 secretion was completely blocked by genistein (PTK inhibitor) or UO126 (MAPK inhibitor). HUVEC stimulation assays, mAb cross-linking, PTK/MAPK inhibitors, Northern blot for IL-8 mRNA, ELISA for IL-8 protein Clinical and experimental immunology Medium 11531942
2000 Murine C1qR(P)/CD93 is expressed in myeloid cell lines but not in a mouse epithelial cell line, parallel to human expression. A polyclonal antibody to a C-terminal peptide common to murine and human CD93 inhibited C1q-enhanced phagocytosis when cells were permeabilized to allow intracellular access, confirming that the intracellular C-terminus is required for phagocytic signal transduction. Northern blot, RT-PCR, Western blot, FACS, cell permeabilization with intracellular antibody, phagocytosis assay Molecular immunology Medium 11074255
1998 CD93/C1qRP mRNA and cell surface protein expression is restricted to cells of myeloid origin (monocytes, macrophages, neutrophils, U937) and endothelial cells, but not lymphoid cells (T, B cell lines), HeLa epithelial cells, smooth muscle cells, or fibroblasts. CD93 protein was also detected in human platelet lysates. Northern blot, RT-PCR, FACS with anti-C1qRP mAbs R139 and R3, Western blot of platelet lysates Journal of immunology Medium 9469455
1994 Three mAbs (R139, R3, U40.3) recognize the same 100 kDa (126 kDa under reducing conditions) surface protein on phagocytic cells (U937, monocytes, neutrophils). R3 and R139 (but not U40.3) inhibit C1q-mediated enhancement of phagocytosis, and R3 partially inhibits [125I]C1q-CLF binding. The three mAbs co-immunoprecipitate CD43 with the receptor, suggesting CD93 may exist in a multi-subunit complex. None of the mAbs inhibit C1q-mediated superoxide production in neutrophils, indicating the phagocytic CD93 receptor is distinct from the superoxide-triggering C1q receptor. Immunoprecipitation, Western blot, functional phagocytosis inhibition assay, radioligand binding inhibition assay, superoxide production assay Journal of immunology High 8144968
2001 A specific sequence motif GE(K/Q/R)GEP in the collagen-like domain of MBL and other defense collagens is critical for triggering CD93-mediated enhancement of phagocytosis. MBL mutants lacking GXY triplets below the kink region (including the GEKGEP sequence) failed to enhance phagocytosis by human monocytes, while wild-type and other mutants retained activity. Baculovirus/Sf9 expression of wild-type and mutant rMBL constructs, phagocytosis enhancement assay with human peripheral blood monocytes Journal of biological chemistry High 11533031
1994 CD93 on human PMN is up-regulated from intracellular stores upon FMLP stimulation in a microtubule-dependent manner (blocked by taxol), indicating CD93 is stored in intracellular vesicles (likely complement receptor exocytic vesicles, CREV). Phorbol myristate acetate causes unimodal up-regulation. The receptor co-localizes in the CREV with CR1 and CR3. Flow cytometry with biotinylated C1q, affinity precipitation from surface-iodinated PMN, taxol treatment, FMLP stimulation Journal of immunology Medium 7911495
2001 CD93/C1qR(P) is predominantly expressed on vascular endothelial cells in human tissues, while it is absent from most tissue macrophages. In vitro differentiation of blood monocytes to dendritic cells causes down-regulation of CD93. A subset of pyramidal neurons in brain also express CD93. Polyclonal antibodies to N- and C-terminal peptides, immunohistochemistry of human tissues, in vitro monocyte-to-dendritic cell differentiation with FACS Journal of leukocyte biology Medium 11698500
2021 CD93 CAR T cells potently kill AML cells in vitro and in vivo and spare hematopoietic stem and progenitor cells (HSPCs), but cause on-target off-tumor toxicity to endothelial cells, which also express CD93. NOT-gated CD93 CAR T cells that express an inhibitory receptor for an endothelial-specific antigen circumvent endothelial cell toxicity in a model system. In vitro cytotoxicity assays, in vivo murine AML models, endothelial cell killing assays, NOT-gate CAR T cell engineering Blood cancer discovery Medium 34778803
2025 CD93 blockade on tumor vasculature increases expression of adhesion molecules ICAM1 and VCAM1, promotes vascular maturation, and improves effector T-cell infiltration into solid tumors. Neutralizing antibodies against ICAM1 and VCAM1 partially reversed the T-cell infiltration benefit. Anti-CD93 selectively promotes T-cell infiltration in tumors where the CD93 pathway is upregulated, and synergizes with adoptive T-cell transfer to inhibit tumor progression. Monoclonal antibody treatment in implanted mouse melanoma models, immunofluorescent staining for vascular maturation markers, flow cytometry for tumor-infiltrating lymphocytes, ICAM1/VCAM1 neutralizing antibody experiments Journal for immunotherapy of cancer Medium 39805660
2024 CD93 in pleural mesothelial cells suppresses CCL21 secretion, thereby reducing dendritic cell migration to lymph nodes and suppressing systemic anti-tumor T-cell responses. Tumor-derived extracellular vesicle miR-5110 downregulates pMC CD93, promoting CCL21 secretion. C1q (elevated in tumor environments) suppresses CD93-mediated CCL21 secretion. Anti-CD93 antibodies inhibit both tumor angiogenesis and promote CCL21 secretion from pMCs. siRNA knockdown, recombinant protein and antibody generation, RNA-Seq, miRNA array, luciferase reporter assay, chemotaxis assay, flow cytometry, EV uptake experiments, ELISA Theranostics Medium 38250037
2002 CD93/C1qR(P) marks a rare human stem cell population with both hematopoietic and hepatic differentiation potential. C1qR(P)+ cells from umbilical cord blood and adult bone marrow include both CD34+ and CD34- bone-marrow-repopulating stem cells, and highly purified lineage-negative CD45+CD38-C1qR(P)+ cells can differentiate into human hepatocytes in NOD/SCID mice. FACS purification, xenograft transplantation into NOD/SCID mice, in vivo hepatic differentiation assay PNAS Medium 12140365
1993 Platelet activation by aggregated C1q multimers (>5 µg/ml) is mediated by the collagenous domain of C1q through the platelet C1qR (67 kDa). Activation results in IP3 release, induction of GPIIb-IIIa (αIIbβ3) fibrinogen receptors, P-selectin expression, granule release, and procoagulant activity. The collagenous domain of C1q (c-C1q) and a monoclonal anti-C1qR antibody inhibit platelet aggregation. Platelet adhesion and aggregation assays, IP3 measurement, fibrinogen binding (Scatchard analysis), P-selectin FACS, kaolin recalcification time, inhibition with c-C1q and anti-C1qR mAb Journal of experimental medicine Medium 7688027

Source papers

Stage 0 corpus · 63 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2000 C1q: structure, function, and receptors. Immunopharmacology 397 10904115
1997 cDNA cloning and primary structure analysis of C1qR(P), the human C1q/MBL/SPA receptor that mediates enhanced phagocytosis in vitro. Immunity 206 9047234
2002 C1qRp defines a new human stem cell population with hematopoietic and hepatic potential. Proceedings of the National Academy of Sciences of the United States of America 136 12140365
1993 Platelet activation by C1q results in the induction of alpha IIb/beta 3 integrins (GPIIb-IIIa) and the expression of P-selectin and procoagulant activity. The Journal of experimental medicine 127 7688027
2004 Murine CD93 (C1qRp) contributes to the removal of apoptotic cells in vivo but is not required for C1q-mediated enhancement of phagocytosis. Journal of immunology (Baltimore, Md. : 1950) 117 15004139
1994 Human T cells express specific binding sites for C1q. Role in T cell activation and proliferation. Journal of immunology (Baltimore, Md. : 1950) 100 8046223
1998 C1qRP, the C1q receptor that enhances phagocytosis, is detected specifically in human cells of myeloid lineage, endothelial cells, and platelets. Journal of immunology (Baltimore, Md. : 1950) 99 9469455
1994 Calreticulin is released from activated neutrophils and binds to C1q and mannan-binding protein. Clinical immunology and immunopathology 96 8062452
1994 Cell-surface protein identified on phagocytic cells modulates the C1q-mediated enhancement of phagocytosis. Journal of immunology (Baltimore, Md. : 1950) 96 8144968
2001 Antibody-mediated phagocytosis of the amyloid beta-peptide in microglia is differentially modulated by C1q. Journal of immunology (Baltimore, Md. : 1950) 89 11390503
2021 NOT-Gated CD93 CAR T Cells Effectively Target AML with Minimized Endothelial Cross-Reactivity. Blood cancer discovery 82 34778803
1984 Identification of the Raji cell membrane-derived C1q inhibitor as a receptor for human C1q. Purification and immunochemical characterization. The Journal of experimental medicine 80 6436431
1997 The C1q and collectin binding site within C1q receptor (cell surface calreticulin). Immunopharmacology 78 9476117
2005 CD93 is rapidly shed from the surface of human myeloid cells and the soluble form is detected in human plasma. Journal of immunology (Baltimore, Md. : 1950) 73 16002728
1995 Murine mast cells express two types of C1q receptors that are involved in the induction of chemotaxis and chemokinesis. Journal of immunology (Baltimore, Md. : 1950) 67 7650391
2000 Structural and functional evidence for microglial expression of C1qR(P), the C1q receptor that enhances phagocytosis. Journal of leukocyte biology 63 10648005
1999 C1qRP is a heavily O-glycosylated cell surface protein involved in the regulation of phagocytic activity. Journal of immunology (Baltimore, Md. : 1950) 58 10092817
2001 Identification of a site on mannan-binding lectin critical for enhancement of phagocytosis. The Journal of biological chemistry 57 11533031
1993 Isolation of a human endothelial cell C1q receptor (C1qR). Journal of leukocyte biology 54 8445329
1990 Platelet C1q receptor interactions with collagen- and C1q-coated surfaces. Journal of immunology (Baltimore, Md. : 1950) 54 2212670
1997 The C1q-binding cell membrane proteins cC1q-R and gC1q-R are released from activated cells: subcellular distribution and immunochemical characterization. Clinical immunology and immunopathology 52 9191880
1990 Interaction of C1q with its receptor on cultured cell lines induces an anti-proliferative response. Clinical immunology and immunopathology 51 2293904
1996 Localisation of the C1q binding site within C1q receptor/calreticulin. FEBS letters 48 8955356
2001 C1qR(P), a myeloid cell receptor in blood, is predominantly expressed on endothelial cells in human tissue. Journal of leukocyte biology 47 11698500
2021 C1q binding to surface-bound IgG is stabilized by C1r2s2 proteases. Proceedings of the National Academy of Sciences of the United States of America 46 34155115
1991 Complement component C1q and its receptor are involved in the interaction of human sperm with zona-free hamster eggs. Molecular reproduction and development 43 1878225
1988 Reversible biotinylation of C1q with a cleavable biotinyl derivative. Application in C1q receptor (C1qR) purification. Journal of immunological methods 41 3259972
2004 CD93 interacts with the PDZ domain-containing adaptor protein GIPC: implications in the modulation of phagocytosis. Journal of leukocyte biology 39 15459234
2011 Plasma CD93 concentration is a potential novel biomarker for coronary artery disease. Journal of internal medicine 37 21332844
1990 Participation of C1q and its receptor in adherence of human diploid fibroblast. Journal of immunology (Baltimore, Md. : 1950) 37 2212651
2005 Modulated interaction of the ERM protein, moesin, with CD93. Immunology 36 15819698
1999 Up-regulation of endothelial cell binding proteins/receptors for complement component C1q by inflammatory cytokines. The Journal of laboratory and clinical medicine 36 10360628
2000 Characterization and molecular cloning of rat C1qRp, a receptor on NK cells. European journal of immunology 33 11093152
2003 Cell surface expression of C1qRP/CD93 is stabilized by O-glycosylation. Journal of cellular physiology 32 12891708
2015 CD93 gene polymorphism is associated with disseminated colorectal cancer. International journal of colorectal disease 30 26008729
2010 A gC1qR prevents white spot syndrome virus replication in the freshwater crayfish Pacifastacus leniusculus. Journal of virology 29 20686021
2016 Elevated expression of CD93 promotes angiogenesis and tumor growth in nasopharyngeal carcinoma. Biochemical and biophysical research communications 28 27255994
1988 Identification and partial characterization of human platelet C1q binding sites. Journal of immunology (Baltimore, Md. : 1950) 27 3183380
1986 Production and characterization of a murine monoclonal IgM antibody to human C1q receptor (C1qR). Journal of immunology (Baltimore, Md. : 1950) 27 3487576
1994 Regulation of C1q receptor expression on human polymorphonuclear leukocytes. Journal of immunology (Baltimore, Md. : 1950) 23 7911495
1994 Characterization of the human neutrophil C1q receptor and functional effects of free ligand on activated neutrophils. Blood 23 8068954
2016 Soluble CD93 as a Novel Biomarker in Asthma Exacerbation. Allergy, asthma & immunology research 19 27334785
2016 Whole Transcriptome Profiling Identifies CD93 and Other Plasma Cell Survival Factor Genes Associated with Measles-Specific Antibody Response after Vaccination. PloS one 19 27529750
2001 C1q-bearing immune complexes induce IL-8 secretion in human umbilical vein endothelial cells (HUVEC) through protein tyrosine kinase- and mitogen-activated protein kinase-dependent mechanisms: evidence that the 126 kD phagocytic C1q receptor mediates immune complex activation of HUVEC. Clinical and experimental immunology 19 11531942
1992 Smooth muscle and epithelial cells express specific binding sites for the C1q component of complement. Clinical immunology and immunopathology 19 1591883
2016 Soluble CD93 Is Involved in Metabolic Dysregulation but Does Not Influence Carotid Intima-Media Thickness. Diabetes 17 27659228
1999 Cloning of the mouse homolog of the 126-kDa human C1q/MBL/SP-A receptor, C1qR(p). Mammalian genome : official journal of the International Mammalian Genome Society 16 10430665
2020 Soluble CD93 in allergic asthma. Scientific reports 15 31941986
2000 Characterization of the murine homolog of C1qR(P): identical cellular expression pattern, chromosomal location and functional activity of the human and murine C1qR(P). Molecular immunology 15 11074255
1993 The C1q-R participates in immunoregulation and signal transduction. Behring Institute Mitteilungen 15 8172572
2012 Augmented production of soluble CD93 in patients with systemic sclerosis and clinical association with severity of skin sclerosis. The British journal of dermatology 14 22540233
1992 Short amino acid sequences derived from C1q receptor (C1q-R) show homology with the alpha chains of fibronectin and vitronectin receptors and collagen type IV. Journal of leukocyte biology 14 1377218
2020 Significance of Soluble CD93 in Type 2 Diabetes as a Biomarker for Diabetic Nephropathy: Integrated Results from Human and Rodent Studies. Journal of clinical medicine 13 32397261
2025 CD93 blockade promotes effector T-cell infiltration and facilitates adoptive cell therapy in solid tumors. Journal for immunotherapy of cancer 9 39805660
2024 Blockade of CD93 in pleural mesothelial cells fuels anti-lung tumor immune responses. Theranostics 8 38250037
2022 CD93 is Associated with Glioma-related Malignant Processes and Immunosuppressive Cell Infiltration as an Inspiring Biomarker of Survivance. Journal of molecular neuroscience : MN 8 36006582
2021 CD93 has a crucial role in pathogenesis of psoriasis. Journal of cosmetic dermatology 5 34028163
2023 CD93 serves as a potential biomarker of gastric cancer and correlates with the tumor microenvironment. World journal of clinical cases 4 36818626
2022 Determining biomarkers for evaluation and diagnosis of hereditary angioedema. Clinical and translational allergy 4 36254341
2024 Immuno-PET Imaging of CD93 Expression with 64Cu-Radiolabeled NOTA-mCD93 ([64Cu]Cu-NOTA-mCD93) and Insulin-Like Growth Factor Binding Protein 7 ([64Cu]Cu-NOTA-IGFBP7). Molecular pharmaceutics 1 39533706
2026 Serum CD93 as a Potential Diagnostic Biomarker for Endometrial Cancer: A Case-Control Study. Journal of clinical medicine 0 42123142
2025 CD93: A Promising NETs-Related Biomarker for Diagnosis and Therapy in Actinic Keratosis. OncoTargets and therapy 0 40901493
2022 Amniotic fluid soluble CD93 is elevated in the presence of intra-amniotic inflammation in preterm prelabor rupture of the fetal membranes. Ceska gynekologie 0 36543585

Missed literature

Know a paper Affinage missed for CD93? Flag it for the maintainers and the community.

No submissions yet.