TREM2 (E9N1K) Rabbit mAb (BSA and Azide Free) #32905

Filter:

ELISA

Supporting Data

REACTIVITY	M
SENSITIVITY	Endogenous
MW (kDa)	28
Source/Isotype	Rabbit IgG

Application Key:

ELISA-ELISA

Species Cross-Reactivity Key:

M-Mouse

Product Information

Product Usage Information

This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.

BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.

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 -20°C. This product will freeze at -20°C 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.

Specificity / Sensitivity

TREM2 (E9N1K) Rabbit mAb (BSA and Azide Free) recognizes endogenous levels of total TREM2 protein.

Species Reactivity:

Mouse

Source / Purification

Monoclonal antibody is produced by immunizing animals with a recombinant protein corresponding to residues around Thr94 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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