R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
CD72 (E4K4A) Rabbit mAb #28182
Filter:
- F
Supporting Data
REACTIVITY | H |
SENSITIVITY | Endogenous |
MW (kDa) | |
Source/Isotype | Rabbit IgG |
Application Key:
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
Application | Dilution |
---|---|
Flow Cytometry (Live) | 1:100 - 1:400 |
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.
Protocol
Specificity / Sensitivity
CD72 (E4K4A) Rabbit mAb recognizes endogenous levels of total CD72 protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gln314 of human CD72 protein.
Background
CD72 is an inhibitory co-receptor of the B cell antigen receptor (BCR) and is expressed primarily on B cells (1,2). The cytoplasmic domain of CD72 contains immunoreceptor tyrosine-based inhibition motifs (ITIMs) that are phosphorylated by Lyn when Lyn associates with BCR (3-5). This phosphorylation leads to recruitment of SHP-1 to CD72 and negative regulation of BCR signaling (4,5). The extracellular portion of CD72 contains a C-type lectin domain, and binding its ligand, CD100/Semaphorin-4D, leads to dissociation of CD72 and SHP-1 and thus relief of BCR signaling suppression (6,7). Recently, Semaphorin-3A was also reported to act as a ligand for CD72; however, unlike CD100/Semaphorin-4D, association with Semaphorin-3A induces CD72 ITAM phosphorylation and association of CD72 with SHP-1 (8). CD72 also plays a role in systemic lupus erythematosus (SLE); through its recognition of the self-antigen Sm/RNP, CD72 suppresses the TLR7-dependent B cell response to nucleic acid self-antigens, inhibiting SLE development (9).
- Wu, Y. et al. (1998) Curr Biol 8, 1009-17.
- Tsubata, T. (2018) Front Immunol 9, 2276.
- Thomas, M.L. (1995) J Exp Med 181, 1953-6.
- Adachi, T. et al. (1998) J Immunol 160, 4662-5.
- Tsubata, T. (2012) Infect Disord Drug Targets 12, 181-90.
- Kumanogoh, A. et al. (2000) Immunity 13, 621-31.
- Ishida, I. et al. (2003) Int Immunol 15, 1027-34.
- Eiza, N. et al. (2023) J Autoimmun 134, 102960.
- Tsubata, T. (2019) Immune Netw 19, e1.
限制使用
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