Render Target: STATIC
Render Timestamp: 2024-12-20T12:00:10.602Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-09-30 01:59:10.240
Product last modified at: 2024-12-17T18:57:12.979Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

CD93/C1qR (E5H9B) Rabbit mAb #55011

Filter:
  • WB
  • IP
  • IHC
  • F

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 120, 82
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IHC-Immunohistochemistry 
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50
    Immunohistochemistry (Paraffin) 1:800 - 1:3200
    Flow Cytometry (Live) 1:400 - 1:1600

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    For a carrier free (BSA and azide free) version of this product see product #55570.

    Protocol

    Specificity / Sensitivity

    CD93/C1qR (E5H9B) Rabbit mAb recognizes endogenous levels of total CD93/C1qR protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the extracellular domain of human CD93/C1qR protein.

    Background

    CD93/complement component C1q receptor (C1qR) is a type-I transmembrane glycoprotein belonging to the CLEC14 family of surface antigens, which share a similar ectodomain architecture highlighted by the presence of a C-type lectin domain and multiple EGF-like domains. CD93/C1qR expression is primarily restricted to endothelial cells associated with normal and tumor-associated vasculature as well as immune cells of the myeloid lineage, including monocytes and neutrophils (1). The extracellular domain of CD93/C1qR is rich in O-linked glycosylation modifications, which stabilizes its surface expression by protecting it from proteolytic cleavage (2,3). CD93/C1qR regulates various aspects of endothelial cell biology, including proliferation, migration, and adhesion (4). Indeed, research studies have demonstrated that surface expressed CD93/C1qR binds to an endothelial specific extracellular matrix ligand, multimerin-2, and disrupting the interaction compromises angiogenesis (5). Furthermore, CD93 expression is upregulated in tumor vasculature and correlates with poor survival (6-8).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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