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Human TREM-2 / TREM2 ELISA Pair Set

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Materials provided
Capture Ab:0.25 mg/mL of rabbit anti-TREM2 monoclonal antibody, Dilute to a working concentration of 2.0 μg/mL in CBS before coating.
Detection Ab:0.5 mg/mL mouse anti-TREM2 monoclonal antibody conjugated to horseradish-peroxidase (HRP). Dilute to working concentration of 0.1 μg/mL in detection antibody dilution buffer before use.
Standard:Each vial contains 100 ng of recombinant TREM2. Reconstitute standard powder with 1 mL detection antibody dilution buffer. After reconstitution, store at -20℃ to -70℃ in a manual defrost freezer. A six-point standard curve usi ng 2-fold serial dilutions in sample dilution buffer, and a high standard of 4000 pg/mL is recommended.
Sensitivity
The minimum detectable dose of Human TREM-2 / TREM2 was determined to be approximately 125 pg/ml. This is defined as at least three times standard deviations above the mean optical density of 10 replicates of the zero standard.
Principle of the product
The Human TREM-2 / TREM2 ELISA Pair Set is for the quantitative determination of Human TREM-2 / TREM2.
This ELISA Pair Set contains the basic components required for the development of sandwich ELISAs.
The Sino Biological ELISA Pair Set is a solid phase sandwich ELISA (Enzyme-Linked Immunosorbent Assay). It utilizes a monoclonal antibody specific for TREM-2 / TREM2 coated on a 96-well plate. Standards and samples are added to the wells, and any TREM-2 / TREM2 present binds to the immobilized antibody. The wells are washed and a horseradish peroxidase conjugated mouse anti-TREM-2 / TREM2 monoclonal antibody is then added, producing an antibody-antigen-antibody "sandwich". The wells are again washed and TMB substrate solution is loaded, which produces color in proportion to the amount of TREM-2 / TREM2 present in the sample. To end the enzyme reaction, the stop solution is added and absorbances of the microwell are read at 450 nm.
Storage
Capture Antibody: Aliquot and store at -20℃ to -70℃ for up to 6 months from date of receipt. Avoid repeated freeze-thaw cycles.
Detection Antibody: Protect it from prolonged exposure to light. Aliquot and store at -20℃ to -70℃ and for up to 6 months from date of receipt. Avoid repeated freeze-thaw cycles.
Standard: Store lyophilized Standard at -20℃ to -70℃ for up to 6 months from date of receipt. Aliquot and store the reconstituted Standard at -20℃ to -70℃ for up to 1 month. Avoid repeated freeze-thaw cycles.
Image
Human TREM-2 / TREM2 ELISA standard curve

Background

Triggering receptor expressed on myeloid cells 2 ( TREM2 ) is a single Ig domain receptor. It is expressed on macrophages and dendritic cells but not on granulocytes or monocytes. Its expression is most abundant in the basal ganglia, corpus callosum, medulla oblongata and spinal cord, and microglial cells are the major TREM2-producing cell type in the central nervous system (CNS). TREM2 may play a role in chronic inflammations and may stimulate production of constitutive rather than inflammatory chemokines and cytokines. TREM2 forms a receptor signaling complex with TYROBP and triggers activation of the immune responses in macrophages and dendritic cells. It also associates with the signal adapter protein, DAP12, which has a cytoplasmic ITAM, leading to the subsequent activation of cytoplasmic tyrosine kinases. TREM2 is both required and sufficient for competent uptake of apoptotic neuronal cells. TREM2 and TREM2-L form a receptor-ligand pair connecting microglia with apoptotic neurons, directing removal of damaged cells to allow repair. Deficiency of the adapter protein DAP12 or its associated receptor TREM2 is associated with abnormal osteoclast development in humans. Defects in TREM2 are causes of PLOSL, also known as NHD. In addition, TREM2 signaling is also an important pathway to promote healing of wounds in the colon where stem cell replacement is necessary.

References
  • Bouchon, A. et al., 2000, J. Immunol. 164: 4991-4995.
  • Paloneva, J. et al., 2002, Am. J. Hum. Genet. 71:656-662. 
  • Prada, I. et al., 2006, Neuroscience. 140 (4): 1139-48.
  • Neumann, H. et al., 2007, J Neuroimmunol. 184 (1-2): 92-9.
  • Thrash, JC. et al., 2009, Neurochem Res. 34 (1): 38-45.
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