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#70551 TREM2 (E9U8L) Rabbit mAb (Amino-terminal Antigen)


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2019年3月22日15時35分 現在
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#70551S100 μL56,000

TREM2 製品一覧

感度分子量 (kDa)抗体の由来貯法
内在性28Rabbit IgG-20℃
種交差性 (社内試験済)
交差する可能性がある種 i


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70551 の推奨プロトコール i

最適な結果を得るために:Cell Signaling Technology (CST) 社は、各製品の推奨プロトコールを使用することを強くお薦めいたします。



ウェスタンブロッティング (1:1000)


TREM2 (E9U8L) Rabbit mAb (Amino-terminal Antigen) recognizes endogenous levels of total TREM2 protein. This protein does not cross-react with mouse TREM2. A non-specific band of unknown origin is observed migrating at ~75 kDa.
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the amino terminus of human TREM2 protein.

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※下記の社内データは、すべて70551 の推奨プロトコールで実験した結果です。

Western Blotting

Western Blotting

Western blot analysis of extracts from THP-1 and SH-SY5Y cells, untreated (-) or treated with peptide N-glycosidase F (PNGase F; +), using TREM2 (E9U8L) Rabbit mAb (Amino-terminal Antigen) (upper) and β-Actin (D6A8) Rabbit mAb #8457 (lower).


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 microglia 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 TREM2 or DAP12 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).

12630   SignalFire™ Plus ECL Reagent
12757   SignalFire™ Elite ECL Reagent
13953   Prestained Protein Marker, Broad Range (11-190 kDa)
6883   SignalFire™ ECL Reagent
7727   Biotinylated Protein Ladder Detection Pack
9997   Tris Buffered Saline with Tween® 20 (TBST-10X)
9999   Nonfat Dry Milk

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TREM2 (E9U8L) Rabbit mAb (Amino-terminal Antigen)

Metabolic Reprogramming in Disease