TREM2 Antibody (08) - Azide and BSA Free

Novus Biologicals, part of Bio-Techne | Catalog # NBP3-21453

Novus Biologicals, part of Bio-Techne

Key Product Details

Species Reactivity

Human

Applications

ELISA, ELISA Detection (Matched Antibody Pair)

Label

Unconjugated

Antibody Source

Monoclonal Mouse IgG1 Clone # 08

Format

Azide and BSA Free

Concentration

Please see the vial label for concentration. If unlisted please contact technical services.

View all TREM2 Antibodies »

Product Specifications

Immunogen

This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human TREM2 (Accession#: NP_061838.1; Met1-Ser174).

Clonality

Monoclonal

Host

Mouse

Isotype

IgG1

Applications for TREM2 Antibody (08) - Azide and BSA Free

Application
Recommended Usage

ELISA

Optimal dilutions of this antibody should be experimentally determined.

ELISA Detection (Matched Antibody Pair)

Optimal dilutions of this antibody should be experimentally determined.

Formulation, Preparation, and Storage

Purification

Protein A purified

Formulation

0.2 um filtered solution in PBS

Format

Azide and BSA Free

Preservative

No Preservative

Concentration

Please see the vial label for concentration. If unlisted please contact technical services.

Shipping

The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.

Stability & Storage

Store at 4C short term. Aliquot and store at -20C long term. Avoid freeze-thaw cycles.

Background: TREM2

Triggering receptor expressed on myeloid cells-2 (TREM2) is a cell surface transmembrane glycoprotein receptor belonging to the immunoglobulin (Ig) subfamily that functions in pathology-induced immune system signaling (1). The TREM2 protein is encoded by the TREM2 gene located on chromosome 6p21.1 in humans and chromosome 17 in mouse (2). TREM2 is synthesized as a protein of 230 amino acids (aa) in length with a theoretic molecular weight (MW) of 25.4 kDa. TREM2 is comprised of a signaling peptide, an extracellular V-type Ig domain, a stalk region, a transmembrane helical domain, and a cytosolic tail (1-4). The receptor is expressed on cells of myeloid lineage including dendritic cells (DCs) and tissue-specific macrophages (e.g. microglia, osteoclasts) (2,3). There are several reported ligands for TREM2 such as bacterial components, lipoproteins, and apolipoproteins (1-3,5). Upon TREM2 receptor-ligand binding, the TREM2 protein interacts with adaptor proteins DNAX activation protein 12 (DAP12) and DAP10 (1-3,5). The TREM2-DAP12 complex leads to phosphorylation of DAP12's immunoreceptor tyrosine-based activation (ITAM) motif, followed by recruitment of Syk kinase, and activation of downstream signaling molecules such as phosphatidylinositol 3-kinase (PI3K), extracellular signal-regulated protein kinase (ERK), and phospholipase Cgamma (PLCgamma) (3,5). A soluble form of TREM2 (sTREM2) is generated by ectodomain shedding via a disintegrin and metalloproteinase 10 (ADAM10) and ADAM17, promoting survival and inflammation through the PI3K and nuclear factor kappa B (NFkappaB) pathways (2,5). TREM2 has been linked to myeloid maturation, proliferation, survival, phagocytosis, response to neurodegenerative cues, and regulation of inflammation (2,3).

TREM2 is upregulated under many pathological conditions and has been of particular interest in neurodegenerative disorders like Alzheimer's disease (AD) where it helps activate microglial responses (1-3,5). Studies have found that sTREM2 is typically elevated in the cerebral spinal fluid (CSF) of AD patients compared to healthy counterparts and may serve as a biomarker of AD (2). While TREM2-mediated microglial activation is considered beneficial in some disease contexts (e.g. demyelinating diseases, ischemia), it is detrimental in others (e.g. peripheral nerve injury) and may be dependent on disease stage, as observed in AD (2,5). Microglia promote amyloid-beta (Abeta) clearance, phagocytosis and reduce tau proliferation in the early stages of AD but can increase Abeta accumulation and tau propagation in late stages of AD (2). Recent studies have also suggested a role for TREM2 in cancer, where it supports an immune-suppressive tumor microenvironment such as reduced of T cell proliferation (1,6). Therapeutic targeting of the TREM2 pathway can be directed towards ligand binding to downstream signaling (1). Potential therapeutic strategies include using monoclonal antibodies or small molecules to either enhance or block signaling (1,6). While more work needs to be done, initial studies targeting TREM2 for cancer immunotherapy is promising (6).

References

1. Deczkowska A, Weiner A, Amit I. The Physiology, Pathology, and Potential Therapeutic Applications of the TREM2 Signaling Pathway. Cell. 2020; 181(6):1207-1217. https://doi.org/10.1016/j.cell.2020.05.003

2. Qin Q, Teng Z, Liu C, Li Q, Yin Y, Tang Y. TREM2, microglia, and Alzheimer's disease. Mech Ageing Dev. 2021; 195:111438. https://doi.org/10.1016/j.mad.2021.111438

3. Kober DL, Brett TJ. TREM2-Ligand Interactions in Health and Disease. J Mol Biol. 2017; 429(11):1607-1629. https://doi.org/10.1016/j.jmb.2017.04.004

4. Uniprot (Q9NZC2)

5. Konishi H, Kiyama H. Microglial TREM2/DAP12 Signaling: A Double-Edged Sword in Neural Diseases. Front Cell Neurosci. 2018; 12:206. https://doi.org/10.3389/fncel.2018.00206

Long Name

Triggering Receptor Expressed on Myeloid Cells 2

Alternate Names

PLOSL2, TREM-2

Gene Symbol

TREM2

Additional TREM2 Products

Product Documents for TREM2 Antibody (08) - Azide and BSA Free

Product Datasheets

Certificate of Analysis

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Product Specific Notices for TREM2 Antibody (08) - Azide and BSA Free

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

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