Human CD300a/LMIR1 Antibody Summary
Applications
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.
Scientific Data
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Human CD300a/LMIR1 ELISA Standard Curve. Recombinant Human CD300a/LMIR1 protein was serially diluted 2-fold and captured by Rat Anti-Human CD300a/LMIR1 Monoclonal Antibody (Catalog # MAB26401) coated on a Clear Polystyrene Microplate (Catalog # DY990). Goat Anti-Human CD300a/LMIR1 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF2640) was biotinylated and incubated with the protein captured on the plate. Detection of the standard curve was achieved by incubating Streptavidin-HRP (Catalog # DY998) followed by Substrate Solution (Catalog # DY999) and stopping the enzymatic reaction with Stop Solution (Catalog # DY994).
Reconstitution Calculator
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: CD300a/LMIR1
CD300a, also known as LMIR1 (in rodents), CMRF-35H, IRp60, CLM-8, and MAIR-I, is a 60 kDa glycoprotein member of the immunoglobulin superfamily (1). Human CD300a consists of a 163 amino acid (aa) extracellular domain (ECD) with one Ig-like V-type domain, a 21 aa transmembrane segment, and a 98 aa cytoplasmic domain that contains three immunoreceptor tyrosine-based inhibitory motifs (ITIMs) and a non-canonical ITIM (2). Alternative splicing may generate additional isoforms that either lack the Ig-like domain or contain only the cytoplasmic domain. Within the ECD, human CD300a shares 40% and 43% aa sequence identity with mouse and rat LMIR1, respectively. In human, CD300a is expressed on peripheral blood eosinophils, mast cells, neutrophils, plasmacytoid dendritic cells, and various T cell subsets (3‑7). Antibody crosslinking of CD300a induces phosphorylation of tyrosine residues in the cytoplasmic domain. This leads to the recruitment of phosphatases SHIP, SHP-1, and SHP-2 and inhibition of NK cell, eosinophil, and mast cell activation (2, 3, 5‑7). Crosslinking of CD300a to other surface proteins such as SCF R or Fc epsilon RI on mast cells, Fc gamma RIIA on neutrophils, or CCR3 on mast cells and eosinophils inhibits downstream signaling from those receptors (5, 10‑12). CD300a crosslinking also limits the in vivo activities of these cells with a subsequent reduction of allergic inflammation symptoms (4, 11, 12).
- Clark, G.J. et al. (2009) Trends Immunol. 30:209.
- Cantoni, C. et al. (1999) Eur. J. Immunol. 29:3148.
- Munitz, A. et al. (2006) Blood 107:1996.
- Bachelet, I. et al. (2005) J. Immunol. 175:7989.
- Alvarez, Y. et al. (2008) Mol. Immunol. 45:253.
- Ju, X. et al. (2008) Blood 112:1184.
- Clark, G.J. et al. (2007) J. Leukoc. Biol. 82:1126.
- Kumagai, H. et al. (2003) Biochem. Biophys. Res. Commun. 307:719.
- Yotsumoto, K. et al. (2003) J. Exp. Med. 198:223.
- Bachelet, I. et al. (2008) J. Immunol. 180:6064.
- Bachelet, I. et al. (2006) J. Allergy Clin. Immunol. 117:1314.
- Munitz, A. et al. (2006) J. Allergy Clin. Immunol. 118:1082.
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