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PDP - Template Name: Matched Antibody Pair
PDP - Template ID: *******446e1e7

TREM2 (Full-length) Matched Antibody Pair #71187

    Supporting Data

    REACTIVITY M
    Application Key:
    • ELISA-ELISA 
    Species Cross-Reactivity Key:
    • M-Mouse 

    Product Information

    Product Usage Information

    Matched Antibody Pairs include capture and detection antibodies to non-overlapping epitopes. Optimal dilutions/concentrations should be determined by the end user.

    Formulation

    Supplied in 1X PBS (10 mM Na2HPO4, 3 mM KCl, 2 mM KH2PO4, and 140 mM NaCl (pH 7.8)). BSA and Azide Free.

    Storage

    Store at -20ºC. This product will freeze at -20ºC so it is recommended to aliquot into single-use vials to avoid multiple freeze/thaw cycles. A slight precipitate may be present and can be dissolved by gently vortexing. This will not interfere with antibody performance.

    Product Description

    The TREM2 (Full-length) Matched Antibody Pair is ideal for use with immunoassay technologies and high-throughput ELISA platforms requiring antibody pairs with specialized or custom antibody labeling. Labels include fluorophores, lanthanides, biotin, and beads. Platforms requiring conjugated Matched Antibody Pairs include MSD, Quanterix Simoa, Alpha Technology (AlphaScreen, AlphaLISA, LANCE, HTRF), and Luminex.

    Learn how Matched Antibody Pairs move your projects forward, faster at cst-science.com/matched-antibody-pairs.

    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 TREM2 or DAP12 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).

    For Research Use Only. Not For Use In Diagnostic Procedures.
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