Detects mouse TREM‑2 in Western blots. In Western blots, approximately 5% cross-reactivity with recombinant human (rh) TREM-2 is observed and less than 1% cross-reactivity with recombinant mouse (rm) TREM-1 and rmTREM-3 is observed.
TREM‑2 was detected in immersion fixed mouse splenocytes using Mouse Anti-TREM‑2 Biotinylated Antigen Affinity-purified Polyclonal Antibody (Catalog # BAF1729) at 10 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Streptavidin (yellow; Catalog # NL999) and counterstained with DAPI (blue). View our protocol for Fluorescent ICC Staining of Non-adherent Cells.
Preparation and Storage
Reconstitute at 0.2 mg/mL in sterile PBS.
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
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.
TREM-2 (Triggering Receptor Expressed by Myeloid cells) is an Ig superfamily cell surface receptor that activates a number of myeloid cell types (1). It is a member of a small gene family located on human chromosome 6p21 and mouse chromosome 17 in a region linked to the MHC (2). A single human TREM-2 gene has been described, however, two closely related orthologs were reported in mouse (3). The proteins differ by only three amino acids and were designated TREM‑2a and TREM‑2b. TREM-2 is type I transmembrane protein consisting of a single extracellular immunoglobulin (V-like) domain, a transmembrane domain with a positively charged lysine residue, and a short cytoplasmic tail (1). It associates with the signal adapter protein, DAP12, for signaling and function. DAP12 has a cytoplasmic ITAM that is phosphorylated upon ligand binding leading to the subsequent activation of cytoplasmic tyrosine kinases. TREM‑2 is expressed by immature monocyte‑derived dendritic cells (DC), and expression is down-regulated upon activation of DC by microbial products and co‑stimulatory signals (4). Ligation of TREM‑2 on immature DC with anti-TREM‑2 antibodies results in partial DC activation and the up-regulation of CCR7 and some co-stimulatory molecules. A role for TREM‑2 in the functioning of osteoclasts and microglia is suggested by the discovery that homozygous loss-of-function mutations in either TREM‑2 or DAP12 result in Nasu-Hakola disease characterized by a combination of presenile demetia and bone cysts (5). In vitro studies indicate that the differentiation of myeloid precursors into osteoclasts is dramatically impaired in TREM‑2 deficient individuals (6).
Colonna, M. (2003) Nature Rev. Immunol. 3:445.
Allcock, R. et al. (2003) Eur. J. Immunol. 33:567.
Daws, M. et al. (2001) Eur. J. Immunol. 31:783.
Bouchon, A. et al. (2001) J. Exp. Med. 194:1111.
Paloneva, J. et al. (2002) Am. J. Hum. Genet. 71:656.
Cella, M. et al. (2003) J. Exp. Med. 198:645.
Triggering Receptor Expressed on Myeloid Cells 2
Entrez Gene IDs:
TREM2; TREM-2; Trem2a; Trem2b; Trem2c; TREM-2triggering receptor expressed on myeloid cells 2a; Triggering receptor expressed on monocytes 2; triggering receptor expressed on myeloid cells 2
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