Flow cytometric analysis of Human CD172a/b expression on human peripheral blood Leukocytes. Human peripheral blood Leukocytes were stained with either FITC Mouse IgG1, κ Isotype Control (Left panel) or SDT FITC Mouse Anti-Human CD172a/b Antibody (Right panel) at 5 μl/test. Flow cytometry and data analysis were performed using BD FACSymphony™ A1 and FlowJo™ software.
Product Details
Product Details
Product Specification
Host | Mouse |
Antigen | CD172a/b |
Synonyms | Tyrosine-protein phosphatase non-receptor type substrate 1; SHP substrate 1; SHPS-1; Brain Ig-like molecule with tyrosine-based activation motifs (Bit); CD172 antigen-like family member A; Inhibitory receptor SHPS-1; Macrophage fusion receptor; MyD-1 antigen; Signal-regulatory protein alpha-1 (Sirp-alpha-1); Signal-regulatory protein alpha-2 (Sirp-alpha-2); Signal-regulatory protein alpha-3 (Sirp-alpha-3); p84; SIRPA; BIT; MFR; MYD1; PTPNS1; SHPS1; SIRP Signal-regulatory protein beta-1; SIRP-beta-1; CD172 antigen-like family member B; CD172b; SIRPB1 |
Location | Cell membrane |
Accession | O00241、P78324 |
Clone Number | S-3431 |
Antibody Type | Mouse mAb |
Isotype | IgG1,k |
Application | FCM |
Reactivity | Hu |
Positive Sample | Human peripheral blood Leukocytes |
Purification | Protein G |
Concentration | 0.2 mg/ml |
Conjugation | FITC |
Physical Appearance | Liquid |
Storage Buffer | PBS, 1% BSA, 0.3% Proclin 300 |
Stability & Storage | 12 months from date of receipt / reconstitution, 2 to 8 °C as supplied |
Dilution
application | dilution | species |
FCM | 5μl per million cells in 100μl volume | Hu |
Background
CD172a (SIRPα) and CD172b (SIRPβ1) are paired immunoglobulin-superfamily transmembrane glycoproteins that regulate myeloid-cell activation: CD172a binds CD47 to deliver inhibitory “don’t-eat-me” signals via SHP-1/2 phosphatases, controlling phagocytosis and dendritic-cell homeostasis, whereas CD172b lacks CD47 affinity and instead partners with the adaptor DAP12 to recruit SYK kinase and provide activating cues during innate immune responses.
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