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The antibody was purified by affinity chromatography and conjugated with PE under optimal conditions. The solution is free of unconjugated PE and unconjugated antibody.
Concentration:
0.2 mg/ml
Storage & Handling:
The antibody solution should be stored undiluted at 4°C and protected from prolonged exposure to light. Do not freeze.
Each lot of this antibody is quality control tested by immunofluorescent staining with flow cytometric analysis. For immunofluorescent staining, the suggested use of this reagent is ≤1.0 µg per million cells in 100 µl volume. It is recommended that the reagent be titrated for optimal performance for each application.
COA:
Enter Lot#:
Application Notes:
Additional reported applications (for the relevant formats) include: in vivo and in vitro blocking of protein C binding1.
Application References:
1. Centelles MN, et al. 2010. Thromb Haemost. 103:1239. (Block)
Mouse endothelial cell line bEnd.3 was stained with CD201 (clone RCR-16) PE (filled histogram) or rat IgG2a, κ PE isotype control (open histogram).
Endothelial protein C receptor (EPCR), also known as CD201, is a 46 kD N-glycosylated type I transmembrane protein, primarily expressed on the endothelial cells of arteries and veins in heart and lung. It is also expressed at high levels on a subset of hematopoietic stem cells and a subset of dendritic cells. CD201 functions as a primary receptor for protein C activation, and results in inhibition of both intrinsic and extrinsic coagulation pathways. It also plays an important role in many pathophysiologic processes, such as inflammation responses to infection, trauma, hematopoiesis, and autoimmune response. Deletion of the CD201 gene in knock-out mice leads to embryonic lethality before embryonic day 10, indicating that CD201 expression is critical for embryo development. In humans, mutations of CD201 have been associated with venous thromboembolism and myocardial infarction as well as with late fetal loss during pregnancy.
Other Names:
Endothelial protein C receptor, protein C receptor, PROCR, activated protein C receptor, APC receptor
Structure:
Type I transmembrane glycoprotein, 46 kD
Distribution:
Endothelial cells, subset of hematopoietic stem cells, subset of dendritic cells
PE anti-mouse CD201 (EPCR), RCR-16, PE, Endothelial protein C receptor, protein C receptor, PROCR, activated protein C receptor, APC receptor, Mouse, Immunology, Antibodies
*These products may be covered by one or more Limited Use Label Licenses (see the BioLegend Catalog or our website, www.biolegend.com/terms). BioLegend products may not be transferred to third parties, resold, modified for resale, or used to manufacture commercial products or to provide a service to third parties without written approval of BioLegend. By use of these products you accept the terms and conditions of all applicable Limited Use Label Licenses. Unless otherwise indicated, these products are for research use only and are not intended for human or animal diagnostic, therapeutic or commercial use.
This data display is provided for general comparisons between formats. Your actual data may vary due to variations in samples, target cells, instruments and their settings, staining conditions, and other factors. If you need assistance with selecting the best format contact our expert technical support team.
Purified anti-mouse CD201 (EPCR)
Mouse endothelial cell line bEnd.3 was stained with CD201 (clone RCR-16) PE (filled histogram) or rat IgG2a, κ PE isotype control (open histogram).
PE anti-mouse CD201 (EPCR)
Mouse endothelial cell line bEnd.3 was stained with CD201 (clone RCR-16) PE (filled histogram) or rat IgG2a, κ PE isotype control (open histogram).
APC anti-mouse CD201 (EPCR)
Mouse endothelial cell line, bEND.3, was stained with mouse CD201 (clone RCR-16) APC (filled histogram) or rat IgG2a, κ APC isotype control (open histogram).
Biotin anti-mouse CD201 (EPCR)
Mouse endothelial cell line, bEND.3, was stained with biotinylated mouse CD201 (clone RCR-16, filled histogram) or rat IgG2a, κ isotype control (open histogram), followed by Sav-PE.