CD93/C1qR (E5H9B) Rabbit mAb (BSA and Azide Free) #55570
- WB
- IHC
- F
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 120, 82 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.
Formulation
Storage
Specificity / Sensitivity
CD93/C1qR (E5H9B) Rabbit mAb (BSA and Azide Free) 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).
- Nepomuceno, R.R. and Tenner, A.J. (1998) J Immunol 160, 1929-35.
- Park, M. and Tenner, A.J. (2003) J Cell Physiol 196, 512-22.
- Ikewaki, N. et al. (2013) Microbiol Immunol 57, 822-32.
- Orlandini, M. et al. (2014) Oncotarget 5, 2750-60.
- Khan, K.A. et al. (2017) Oncogene 36, 6097-6108.
- Bao, L. et al. (2016) Biochem Biophys Res Commun 476, 467-474.
- Langenkamp, E. et al. (2015) Cancer Res 75, 4504-16.
- Sun, Y. et al. (2021) Sci Transl Med 13, eabc8922. doi: 10.1126/scitranslmed.abc8922.
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