Render Target: STATIC
Render Timestamp: 2024-10-04T09:39:49.515Z
Commit: f04ddd7fea9fb3592f59f61482fcb94610d25cbe
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77

TREM2 (E4F5G) Mouse mAb #29715

Filter:
  • WB
  • IF
  • F

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 28
    Source/Isotype Mouse IgG2b kappa
    Application Key:
    • WB-Western Blotting 
    • IF-Immunofluorescence 
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunofluorescence (Immunocytochemistry) 1:50 - 1:200
    Flow Cytometry (Fixed/Permeabilized) 1:100 - 1:400
    Flow Cytometry (Live) 1:100 - 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

    Specificity / Sensitivity

    TREM2 (E4F5G) Mouse mAb 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 Asp140 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 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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