CST, 95410S, TREM2 (Extracellular Amino-terminal Antigen) Matched Antibody Pair

Matched Antibody Pair for studying TREM2 mouse in the research area. Product Usage Information Matched Antibody Pairs consist of capture and detection antibodies that bind to non-overlapping epitopes. For specific identification of the capture and detection antibodies in this pair, please refer to the data figure caption. Optimal dilutions/concentrations should be determined by the end user. Formulation Supplied in 1X PBS (10 mM Na 2 HPO 4 , 3 mM KCl, 2 mM KH 2 PO 4 , and 140 mM NaCl (pH 7.8)). BSA and Azide Free. Storage Store at -20ºC. This product will freeze at -20ºC 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. 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 or 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).t Alternate Names OTTMUSP00000023119; Trem; TREM-2; Trem2; Trem2a; Trem2b; Trem2c; Triggering receptor expressed on monocytes 2; Triggering receptor expressed on myeloid cells 2; triggering receptor expressed on myeloid cells 2a; triggering receptor expressed on myeloid cells 2b; triggering receptor expressed on myeloid cells 2c Specification REACTIVITY: M