R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
TREM2 (D8I4C) Rabbit mAb #91068
Filter:
- WB
- IP
- IF
- F
Supporting Data
REACTIVITY | H |
SENSITIVITY | Endogenous |
MW (kDa) | 28 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IF-Immunofluorescence
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
Application | Dilution |
---|---|
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
Specificity / Sensitivity
TREM2 (D8I4C) Rabbit 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 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 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).
- Colonna, M. (2003) Nat Rev Immunol 3, 445-53.
- Jonsson, T. et al. (2013) N Engl J Med 368, 107-16.
- Boutajangout, A. and Wisniewski, T. (2013) Int J Cell Biol 2013, 576383.
- Wang, Y. et al. (2015) Cell 160, 1061-71.
- Melchior, B. et al. (2010) ASN Neuro 2, e00037.
- Klünemann, H.H. et al. (2005) Neurology 64, 1502-7.
- Thornton, P. et al. (2017) EMBO Mol Med 9, 1366-1378.
- Schlepckow, K. et al. (2017) EMBO Mol Med 9, 1356-1365.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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