Mouse CD177 Alexa Fluor® 488-conjugated Antibody Summary
Accession # Q8R2S8
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Detection of CD177 in Mouse Bone Marrow Cells by Flow Cytometry. Mouse bone marrow cells were stained with Rat Anti-Mouse Gr‑1/Ly‑6G APC‑conjugated Monoclonal Antibody (Catalog # FAB1037A) and either (A) Rabbit Anti-Mouse CD177 Alexa Fluor® 488‑conjugated Monoclonal Antibody (Catalog # FAB8186G) or (B) Normal Rabbit IgG Alexa Fluor 488 Control (Catalog # IC105G). View our protocol for Staining Membrane-associated Proteins.
Preparation and Storage
- 12 months from date of receipt, 2 to 8 °C as supplied.
CD177 is a member of the uPAR/CD59/Ly6 superfamily (1). Mature mouse CD177 is a 796 amino acid (aa) protein that contains four uPAR/Ly6 domains, while human CD177 contains only two. Within common regions, mouse CD177 shares 55% and 77% aa sequence identity with human and rat CD177, respectively. CD177 is expressed on the surface of neutrophils through a glycosylphosphatidylinositol (GPI) anchor (2-4). It is nearly absent from neutrophils from paroxysmal nocturnal hemoglobinurea patients who are deficient in the ability to synthesize GPI linkages (4, 5). It is up-regulated on granulocytes from polycythemia vera and thalassemia patients (6, 7). CD177 binds to PECAM-1 on vascular endothelial cells, an interaction which mediates neutrophil adhesion to the vascular wall and neutrophil transmigration (8). It associates in cis with the Integrin MAC-1 (CD11b/CD18) (9). CD177 also associates in cis with Proteinase 3 (PR3) and is required for cell surface PR3 expression (9-11). PR3 is normally found in intracellular vesicles, but once at the cell surface it can serve as an autoimmune target for anti-neutrophil cytoplasmic antibodies (ANCA) (12). The ANCA targeting of CD177-PR3 complexes triggers neutrophil activation and vasculitis (9, 12).
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- van Timmeren, M.M. and P. Heeringa (2012) Curr. Opin. Rheumatol. 24:8.
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