HEK293 TREM2 DAP12 Cell Line
Item | Cat# | Price |
Stable Cell Line | SNB-OT-0003 | $29,800 |
Compound Testing Services | CT-001 | $1,850 per 384w plate (Up To 16 cpds Dose) |
Product Description
TREM2 (Triggering receptor expressed on myeloid cells 2) refers to a class of activating immune receptor complexes that signal through DAP12 (also known as TYROBP), an adaptor protein containing an ITAM (immunoreceptor tyrosine-based activation motif). DAP12 is widely expressed in myeloid cells such as macrophages, dendritic cells, microglia, and NK cells, and functions as a critical signaling hub for various paired receptors lacking intrinsic signaling domains. Within TREM2 complexes, ligand binding to the extracellular receptor chain triggers phosphorylation of DAP12 ITAM motifs by Src-family kinases, leading to recruitment of Syk/ZAP-70 and activation of downstream cascades including PI3K, PLCγ, and MAPK pathways. These signals regulate phagocytosis, cytokine production, cell activation, and cytoskeletal remodeling. DAP12-associated TREM2 receptors play important roles in host defense, neuroimmune interactions, bone homeostasis, and inflammatory responses, and dysregulation of DAP12 signaling has been linked to autoimmune diseases and neurodegenerative disorders.
Screeningbio’s HEK293 Human TREM2 DAP12 cell line stable express TREM2 DAP12 protein. Upon stimulated, signal pathway was activated and induce pSYK level increase and downstream signal. This cell line is an ideal tool to study compound’s effect against TREM2.
Product Specifications
Target Type | TREM2/DAP12 |
Species | Human |
HGNC Symbol | TREM2/DAP12 |
Accession Number | NM_018965/NM_003332 |
Parental Line | HEK293 |
Lot# | See Vial |
Storage | Liquid Nitrogen |
Data
Target Background
Triggering receptor expressed on myeloid cells 2 (TREM2) and its signaling adaptor DAP12 form a key immunoregulatory receptor complex primarily expressed on microglia, macrophages, osteoclasts, and other tissue-resident myeloid cells. TREM2 is an immunoglobulin-like receptor that recognizes a broad range of endogenous ligands, including lipids, lipoproteins, apoptotic cell components, and microbial products. Because TREM2 has a short cytoplasmic tail lacking signaling motifs, it requires association with DAP12, a transmembrane adaptor protein containing an immunoreceptor tyrosine-based activation motif (ITAM). Upon ligand binding, DAP12 ITAMs are phosphorylated by Src-family kinases, recruiting Syk and initiating downstream cascades involving PI3K, PLCγ, and ERK. These pathways promote cell survival, phagocytosis, lipid metabolism, and anti-inflammatory functions.
The TREM2–DAP12 axis plays a central role in microglial homeostasis in the central nervous system. Loss-of-function mutations in TREM2 or DAP12 lead to impaired microglial activation and phagocytosis, contributing to neurodegenerative conditions such as Alzheimer’s disease, Nasu–Hakola disease, and frontotemporal dementia. In Alzheimer’s pathology, TREM2 signaling enhances microglial clustering around amyloid plaques, improving debris clearance and limiting neurotoxicity. Beyond the CNS, TREM2–DAP12 influences macrophage polarization, metabolic inflammation, and osteoclast differentiation.
Given its involvement in immune regulation and neurodegeneration, the TREM2–DAP12 pathway has become an attractive therapeutic target, with multiple agonistic antibodies and modulators currently under investigation.