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Render Timestamp: 2024-11-22T11:11:49.476Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-30 01:58:51.626
Product last modified at: 2024-11-11T21:30:09.774Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
  1. Products /
  2. Primary Antibodies /
  3. TREM2 (E9O9F) Rabbit mAb
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

TREM2 (E9O9F) Rabbit mAb #59621

Filter:
  • WB

    Supporting Data

    REACTIVITY M
    SENSITIVITY Endogenous
    MW (kDa) 28
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • M-Mouse 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    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 (E9O9F) Rabbit mAb recognizes endogenous levels of total TREM2 protein.

    Species Reactivity:

    Mouse

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the amino terminus of mouse 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).

    Database Links

    UniProt ID: Q99NH8


    Entrez-Gene Id: 83433


    Limited Uses

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