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PathScan® RP TREM2 (Extracellular Amino-terminal Antigen) Sandwich ELISA Kit

PathScan^® RP TREM2 (Extracellular Amino-terminal Antigen) Sandwich ELISA Kit #90595

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Supporting Data

REACTIVITY

Application Key:

ELISA-ELISA

Species Cross-Reactivity Key:

H-Human

Product Information

Product Description

The rapid protocol (RP) PathScan^® RP TREM2 (Extracellular Amino-terminal Antigen) Sandwich ELISA Kit is a solid phase sandwich enzyme-linked immunosorbent assay (ELISA) that detects endogenous levels of TREM2 protein in a reduced assay time of 1.5 hours. Incubation of cell lysates and detection antibody on the coated microwell plate forms a sandwich with TREM2 in a single step. The plate is then extensively washed and TMB reagent is added for signal development. The magnitude of absorbance for the developed color is proportional to the quantity of TREM2 protein. Learn more about your ELISA kit options here.

*Antibodies in this kit are custom formulations specific to kit.

Protocol

Specificity / Sensitivity

The PathScan^® RP TREM2 (Extracellular Amino-terminal Antigen) Sandwich ELISA Kit detects endogenous levels of TREM2 protein. The kit sensitivity is shown in Figures 1 and 2. This kit detects proteins from the indicated species, as determined through in-house testing, but may also detect homologous proteins from other species. The antibodies used in this kit target the extracellular amino-terminal region of human TREM2.

Species Reactivity:

Human

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: Q9NZC2

Entrez-Gene Id: 54209

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

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PathScan® RP TREM2 (Extracellular Amino-terminal Antigen) Sandwich ELISA Kit #90595