Human/Mouse TREM2 Alexa Fluor® 350-conjugated Antibody

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.

Preparation and Storage

Background: TREM2

TREM-2 (Triggering Receptor Expressed on Myeloid cells-2) is a 35 kDa molecular weight type I transmembrane member of the TREM family and Ig superfamily. 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. Within the ECD, human TREM-2 shares 73% and 74% aa sequence identity with mouse and rat TREM-2, respectively. Two closely related transcripts were reported in mouse and designated TREM-2a and TREM-2b. 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. It is a pattern recognition receptor that binds anionic ligands. A positively charged lysine within the transmembrane segment allows association with the signal adapter protein, DAP12 to deliver an activating signal that plays a role in both innate and adaptive immune responses, including inhibition of macrophage activation. TREM-2 is expressed on macrophages, immature myeloid dendritic cells, osteoclasts, microglia, and adipocytes. It promotes the differentiation and function of osteoclasts, the production of inflammatory cytokines by adipocytes, insulin resistance, and the phagocytic clearance of bacteria. 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. TREM-2 also interacts with and modifies signaling through Plexin A1 on dendritic cells and osteoclasts. 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. 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.

Product Datasheets

Product Specific Notices

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Related Research Areas

• Dendritic Cell Activation
• Microglia Activation Markers
• Microglia Homeostasis
• Monocyte Markers
• Semaphorins, Plexin Receptors, and Related Molecules
• Uptake of Amyloid beta by Glia Cells