TREM2 Antibody [F18K20] | Primary Antibodies

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000 IP1:50 IF1:200 - 1:800 FCM1:400

Application
WB, IP, IF, FCM

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
28 kDa

Datasheet & SDS

Biological Description

Specificity
TREM2 Antibody [F18K20] detects endogenous levels of total TREM2 protein.

Clone
F18K20

Synonym(s)
Triggering receptor expressed on myeloid cells 2, TREM-2, Triggering receptor expressed on monocytes 2, TREM2

Background
TREM2 (triggering receptor expressed on myeloid cells 2) is a type I transmembrane immunoreceptor of the TREM family that is highly and selectively expressed on microglia in the CNS as well as on peripheral myeloid cells, where it acts as a lipid- and damage-associated pattern recognition receptor that couples extracellular sensing of apolipoproteins, phospholipids, and amyloid species to intracellular DAP12–SYK–PI3K signaling programs controlling microglial survival, metabolism, chemotaxis, and phagocytosis. The receptor comprises an N‑terminal V‑type Ig-like ectodomain that binds ligands including ApoE, ApoJ/CLU, anionic and aminophospholipids, and multiple forms of amyloid‑β, a single-pass transmembrane segment that associates with the ITAM-bearing adaptor DAP12, and a short cytoplasmic tail that relies on DAP12 for signal propagation; ectodomain shedding at the H157/S158 site generates a soluble TREM2 fragment with distinct signaling properties. Ligand engagement stabilizes TREM2–DAP12 complexes and promotes phosphorylation of the DAP12 ITAM, recruitment and activation of SYK, and downstream activation of PI3K–AKT–mTOR, ERK, and PLCγ pathways, which together enhance microglial survival, proliferation, and metabolic reprogramming, drive chemotactic responses toward amyloid deposits or damaged myelin, and induce a transcriptional switch from homeostatic to disease-associated microglia characterized by upregulation of genes involved in phagocytosis, lipid handling, lysosomal function, and complement. TREM2 supports microglial clustering around plaques, compaction of amyloid cores, and efficient phagocytic clearance of Aβ aggregates and dystrophic neurites, whereas TREM2 deficiency or expression of hypomorphic variants reduces microglial proliferation and plaque encasement, leads to more diffuse and neurotoxic plaque morphology, increases neuritic damage, and accelerates both amyloid deposition and tau seeding and spread. Rare missense variants such as R47H and loss-of-function mutations in TREM2 confer substantially increased risk of late‑onset Alzheimer’s disease and cause Nasu–Hakola disease when biallelic, and mechanistic analyses indicate that these variants reduce ligand binding and/or surface expression, blunt DAP12–SYK signaling, and impair acquisition of the disease-associated microglial phenotype required for effective containment of Aβ and tau pathology.

Background

TREM2 (triggering receptor expressed on myeloid cells 2) is a type I transmembrane immunoreceptor of the TREM family that is highly and selectively expressed on microglia in the CNS as well as on peripheral myeloid cells, where it acts as a lipid- and damage-associated pattern recognition receptor that couples extracellular sensing of apolipoproteins, phospholipids, and amyloid species to intracellular DAP12–SYK–PI3K signaling programs controlling microglial survival, metabolism, chemotaxis, and phagocytosis. The receptor comprises an N‑terminal V‑type Ig-like ectodomain that binds ligands including ApoE, ApoJ/CLU, anionic and aminophospholipids, and multiple forms of amyloid‑β, a single-pass transmembrane segment that associates with the ITAM-bearing adaptor DAP12, and a short cytoplasmic tail that relies on DAP12 for signal propagation; ectodomain shedding at the H157/S158 site generates a soluble TREM2 fragment with distinct signaling properties. Ligand engagement stabilizes TREM2–DAP12 complexes and promotes phosphorylation of the DAP12 ITAM, recruitment and activation of SYK, and downstream activation of PI3K–AKT–mTOR, ERK, and PLCγ pathways, which together enhance microglial survival, proliferation, and metabolic reprogramming, drive chemotactic responses toward amyloid deposits or damaged myelin, and induce a transcriptional switch from homeostatic to disease-associated microglia characterized by upregulation of genes involved in phagocytosis, lipid handling, lysosomal function, and complement. TREM2 supports microglial clustering around plaques, compaction of amyloid cores, and efficient phagocytic clearance of Aβ aggregates and dystrophic neurites, whereas TREM2 deficiency or expression of hypomorphic variants reduces microglial proliferation and plaque encasement, leads to more diffuse and neurotoxic plaque morphology, increases neuritic damage, and accelerates both amyloid deposition and tau seeding and spread. Rare missense variants such as R47H and loss-of-function mutations in TREM2 confer substantially increased risk of late‑onset Alzheimer’s disease and cause Nasu–Hakola disease when biallelic, and mechanistic analyses indicate that these variants reduce ligand binding and/or surface expression, blunt DAP12–SYK signaling, and impair acquisition of the disease-associated microglial phenotype required for effective containment of Aβ and tau pathology.

References
https://pubmed.ncbi.nlm.nih.gov/30532704/ https://pubmed.ncbi.nlm.nih.gov/38020891/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%