TREM-2 ELISA KITS, TRIGGERING RECEPTOR EXPRESSED ON MYELOID CELLS 2 (Parts m, r, c TREM2-ELISA)

TREM-2 ELISA KITS, TRIGGERING RECEPTOR EXPRESSED ON MYELOID CELLS 2

Separate kits available for canine, mouse and rat. Please inquire for human kit

Sandwich ELISA format (96T)

Highlights

Assay ranges 15 to 600 pg/ml depending on species.
13-19 pg/ml sensitivity
Separate kits are available for mouse, rat and canine.
Sandwich ELISA format providing convenience and high sensitivity.
Strip plate format allowing separate use and storage of sections of the ELISA plate.
Rapid protocol: Only one incubation with sample to antibodies. Total protocol time approximately 1.5 hrs.
Colormetric detection at 450nm using a standard absorbance plate reader.

Lead time approximately 2 weeks.

Icon image:

Protocol

Price (USD)	Number of Kits	Number of Assays
$655	1	96T

Specifications (All kits are 96T):

Species	Part	Standard	Assay Range	Sensitivity
Mouse	m-TREM2-ELISA	4800 pg/ml	15-4000 pg/ml	13.2 pg/ml
Rat	r-TREM2-ELISA	4800 pg/ml	15-4000 pg/ml	13.2 pg/ml
Canine	c-TREM2-ELISA	6400 pg/ml	25 - 6000 pg/ml	19.625 pg/ml

Kit Contents

8 x 12 well removable section strip plate coated with anti-TREM2 antibody
Anti-TREM2 polyclonal detection antibody conjugated with biotin
Steptavidin-HRP
Protein Standard
Standard diluent
Concentrated wash solution
Chromogen solutions A and B
Stop solution
Plate sealers

Triggering Receptor Expressed On Myeloid Cells 2 (TREM2).

TREM2 stands for Triggering Receptor Expressed on Myeloid Cells 2. It is a cell surface receptor protein that is expressed on microglia, which are the immune cells of the brain. TREM2 plays an important role in microglial function, including activation, phagocytosis, and cytokine production.

Microglia are responsible for clearing away damaged cells and debris from the brain. They also play a role in inflammation and immunity. TREM2 helps microglia to sense and respond to damage and inflammation in the brain.

TREM2 is particularly important in the context of Alzheimer's disease (AD). AD is a neurodegenerative disease that is characterized by the accumulation of amyloid beta plaques and tau tangles in the brain. Microglia play a key role in clearing away amyloid beta plaques, and TREM2 is essential for this process.

Mutations in the TREM2 gene are associated with an increased risk of AD. These mutations can lead to a loss of TREM2 function, which can impair the ability of microglia to clear away amyloid beta plaques and other debris from the brain.

In addition to its role in AD, TREM2 is also involved in other neurological disorders, such as Parkinson's disease, multiple sclerosis, and amyotrophic lateral sclerosis (ALS). It is also thought to play a role in cancer and other diseases.

Here are some of the specific functions of TREM2:

Microglial activation: TREM2 helps to activate microglia in response to damage and inflammation in the brain.

Phagocytosis: TREM2 helps microglia to phagocytose (engulf and destroy) damaged cells and debris.

Cytokine production: TREM2 helps to regulate the production of cytokines, which are signaling molecules that play a role in inflammation and immunity.

Amyloid beta plaque clearance: TREM2 is essential for microglia to clear away amyloid beta plaques from the brain.

Myeloid cells express receptors belonging to the Immunoglobulin (Ig) superfamily, including TREM2. Homozygous mutations in TREM2 are known to cause rare, early onset autosomal recessive forms of dementia. A rare missense mutation (rs75932628-T) in the gene encoding TREM2, (predicted to result in an R47H substitution), confers a significant risk of Alzheimer's disease. Given the reported antiinflammatory role of TREM2 in the brain, it is suspected of interfering with the brain’s ability to prevent the buildup of plaque. TREM2 mutations increase the risk of neurodegenerative conditions such as Alzheimer's disease, amyotrophic lateral sclerosis, and Parkinson's disease. TREM2 interacts with DAP12 in microglia to trigger phagocytosis of amyloid beta peptide and apoptotic neurons without inflammation. Mutations in TREM2 impair the normal proteolytic maturation of the protein which in turn interferes with phagocytosis and may therefore contribute to the pathogenesis of Alzheimer's disease.

Soluble TREM2 has been detected in human cerebrospinal fluid (CSF), where it was found to be elevated in CSF of patients with multiple sclerosis and other inflammatory neurological conditions in comparison to patients without inflammatory neurologic disorders.

Methods Overview:

The included ELISA micro-strip plate is provided pre-coated with an a monoclonal capture antibody selective to the antigen. Samples are pre-mixed with a biotin-linked detection antibody and streptavidin-HRP, which are then added to the plate. The plate is washed after a 60 min incubation period. Color reagents are added, resulting in a reaction with HRP that yields a blue colored solution. A stop solution is applied to terminate the reaction, and the solution is measured at 450nm.

Sandwich ELISA Methods

ELISA Assay Steps

Mix sample, biotinylated-detection antibody and streptavidin-HRP.
Apply sample and antibody-HRP complex to ELISA plate for 60min at 37^oC. Wash 5 times.
Apply chromogens, incubate, then stop reaction.