Description
Product Usage Information
Western Blotting: 1:1000
Simple Western™: 1:50 - 1:250
Immunoprecipitation: 1:50
Immunofluorescence (Immunocytochemistry): 1:200 - 1:800
Flow Cytometry (Fixed/Permeabilized): 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
Available protocols: Western Blotting, Immunoprecipitation, Immunofluorescence (Immunocytochemistry), Flow Cytometry (Fixed/Permeabilized)
Specificity / Sensitivity
TREM2 (D8I4C) Rabbit Monoclonal Antibody recognizes endogenous levels of total TREM2 protein.
Species Reactivity: Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu221 of human TREM2 protein.
Background
The triggering receptor expressed on myeloid cells 2 (TREM2) protein is an innate immune receptor that is expressed on the cell surface of microglia, macrophages, osteoclasts, and immature dendritic cells (1). The TREM2 receptor is a single-pass type I membrane glycoprotein that consists of an extracellular immunoglobulin-like domain, a transmembrane domain, and a cytoplasmic tail. TREM2 interacts with the tyrosine kinase-binding protein DAP12 to form a receptor-signaling complex (2). The TREM2 protein plays a role in innate immunity and a rare functional variant (R47H) of TREM2 is associated with the late-onset risk of Alzheimer's disease (1,3). Research studies using mouse models of Alzheimer's disease indicate that deficiency and haploinsufficiency of TREM2 can lead to increased β-amyloid (Aβ) accumulation as a result of dysfunctional microglial response (4). These results agree with the distribution of TREM2 in human brain regions (e.g., white matter, the hippocampus, and neocortex) that are involved in Alzheimer's disease pathology (2). In addition, amyloid plaque formation induces expression of TREM2 and amyloid phagocytosis (5). Loss-of-function mutations in the corresponding or genes can result in Nasu-Hakola disease, a rare form of progressive presenile dementia that results from polycystic osseous lesions (6). TREM2 membrane shedding occurs by cleavage at the extracellular site between H157/S158, generating an N-terminal shedded fragment and a membrane bound C-terminal fragment (7,8).t
Alternate Names
PLOSL2; TREM-2; TREM2; Trem2a; Trem2b; Trem2c; Triggering receptor expressed on monocytes 2; Triggering receptor expressed on myeloid cells 2; triggering receptor expressed on myeloid cells 2a
