Human TREM2 Antibody

Catalog #: MAB18282 Datasheet / COA / SDS

Catalog #	Availability	Size / Price	Qty
MAB18282-100
MAB18282-SP

Detection of TREM2 in Human Brain Medulla (Locus Coeruleus).

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Human TREM2 Antibody Summary

Specificity

Detects Human Trem-2 in direct and capture ELISAs

Source

Monoclonal Mouse IgG₁ Clone # 1057114

Purification

Protein A or G purified from hybridoma culture supernatant

Immunogen

NS0-derived recombinant human TREM-2 protein
His19-Ser174

Formulation

Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied either lyophilized or as a 0.2 µm filtered solution in PBS.

Label

Unconjugated

Applications

Recommended Concentration

Sample

Immunohistochemistry

5-25 µg/mL

Immersion fixed paraffin-embedded sections of Human Brain Medulla (Locus Coeruleus)

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

Immunohistochemistry

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Detection of TREM2 in Human Brain Medulla (Locus Coeruleus). TREM2 was detected in immersion fixed paraffin-embedded sections of Human Brain Medulla (Locus Coeruleus) using Mouse Anti-Human TREM2 Monoclonal Antibody (Catalog # MAB18282) at 5 µg/mL for 1 hour at room temperature followed by incubation with the Anti-Mouse IgG VisUCyte™ HRP Polymer Antibody (Catalog # VC001). Before incubation with the primary antibody, tissue was subjected to heat-induced epitope retrieval using VisUCyte Antigen Retrieval Reagent-Basic (Catalog # VCTS021). Tissue was stained using DAB (brown) and counterstained with hematoxylin (blue). Specific staining was localized to cytoplasm in neurons. View our protocol for IHC Staining with VisUCyte HRP Polymer Detection Reagents.

Reconstitution Calculator

Preparation and Storage

Reconstitution

Reconstitute at 0.5 mg/mL in sterile PBS.

Shipping

The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C

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.

Background: TREM2

TREM-2 (Triggering Receptor Expressed on Myeloid cells-2) is a 35 kDa type I transmembrane member of the TREM family and Ig superfamily (1). Mature human TREM-2 consists of a 156 amino acid (aa) extracellular domain (ECD) with one V-type Ig-like domain, a 21 aa transmembrane (TM) domain, and a 35 aa cytoplasmic tail (2). Within the ECD, human TREM-2 shares 73% and 74% aa sequence identity with mouse and rat TREM-2, respectively. Soluble forms of the TREM-2 ECD are generated by alternative splicing or proteolytic cleavage, and the cytoplasmic domain can be liberated by gamma-Secretase mediated intramembrane cleavage (3). A positively charged lysine within the transmembrane segment allows association with the signal adapter protein, DAP12 and inhibition of macrophage activation (4, 5). TREM-2 is expressed on macrophages, immature myeloid dendritic cells, osteoclasts, microglia, and adipocytes (5-9). It promotes the differentiation and function of osteoclasts, the production of inflammatory cytokines by adipocytes, insulin resistance, and the phagocytic clearance of bacteria (9-11). In the CNS, TREM-2 binds to ApoE, ApoA1, and ApoB and mediates the clearance of apoptotic neurons, amyloid plaques, and cell debris following demyelination (6-8, 12). TREM-2 also interacts with and modifies signaling through Plexin A1 on dendritic cells and osteoclasts (13). Mutations in TREM-2 or DAP12 are associated with the development of Alzheimer's disease and Nasu-Hakola disease (NHD/PLOSL) which is characterized by presenile dementia and bone cysts (14, 15). Soluble TREM-2 is elevated in cerebrospinal fluid of patients with active multiple sclerosis (MS), and TREM-2 blockade exacerbates disease symptoms in the experimental EAE model of MS (16, 17).

References

Painter, M.M. et al. (2015) Mol. Neurodegener. 10:43.
Bouchon, A. et al. (2000) J. Immunol. 164:4991.
Wunderlich, P. et al. (2013) J. Biol. Chem. 288:33027.
Hamerman, J.A. et al. (2006) J. Immunol. 177:2051.
Turnbull, I.R. et al. (2006) J. Immunol. 177:3520.
Akahashi, K. et al. (2005) J. Exp. Med. 201:647.
Atagi, Y. et al. (2015) J. Biol. Chem. 290:26043.
Wang, Y. et al. (2016) J. Exp. Med. 213:667.
Cella, M. et al. (2003) J. Exp. Med. 198:645.
Park, M. et al. (2015) Diabetes 64:117.
N'Diaye, E-N. et al. (2009) J. Cell Biol. 184:215.
Poliani, P.L. et al. (2015) J. Clin. Invest. 125:2161.
Akegahara, N. et al. (2006) Nat. Cell Biol. 8:615.
Colonna, M. and Y. Wang (2016) Nat. Rev. Neurosci. 17:201.
Paloneva, J. et al. (2002) Am. J. Hum. Genet. 71:656.
Piccio, L. et al. (2008) Brain 131:3081.
Piccio, L. et al. (2007) Eur. J. Immunol. 37:1290.

Long Name

Triggering Receptor Expressed on Myeloid Cells 2

Entrez Gene IDs

54209 (Human); 102133279 (Cynomolgus Monkey)

Alternate Names

PLOSL2; 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