Western Blot: TREM2 Antibody (2B5) [NBP1-07101] - The cell lysates (40ug) were resolved by SDS-PAGE, transferred to PVDF membrane and probed with TREM2 antibody (1:1000). Proteins were visualized using a goat anti-mouse ...read more
Immunocytochemistry/ Immunofluorescence: TREM-2 Antibody (2B5) [NBP1-07101] - Analysis of TREM2 in Raw264.7 cells line, stained with DAPI (Blue) for nucleus staining and monoclonal anti-human TREM2 antibody (1:100) with ...read more
Flow Cytometry: TREM-2 Antibody (2B5) [NBP1-07101] - Flow cytometry analysis of TREM2 in Hep3B cell line, staining at 2-5ug for 1x106cells. The secondary antibody used goat anti-mouse IgG Alexa fluor 488 conjugate.
Immunocytochemistry/ Immunofluorescence: TREM-2 Antibody (2B5) [NBP1-07101] - HepG2 cells line, stained with DAPI (Blue) for nucleus staining and monoclonal anti-human TREM2 antibody (1:100) with goat anti-mouse ...read more
In Simple Western only 10 - 15 uL of the recommended dilution is used per data point. See Simple Western Antibody Database for Simple Western validation: Tested in MCF-7 lysate 0.5 mg/mL, separated by Size, antibody dilution of 1:10, apparent MW was 45 kDa. Use in IHC-P reported in scientific literature (PMID: 23830013).
Publications
Read Publications using NBP1-07101 in the following applications:
Use in Rat reported in scientific literature (PMID:32139718).
Packaging, Storage & Formulations
Storage
Store at 4C short term. Aliquot and store at -20C long term. Avoid freeze-thaw cycles.
Buffer
PBS (pH 7.4), 10% Glycerol
Preservative
0.02% Sodium Azide
Concentration
1.0 mg/ml
Purity
Protein G purified
Alternate Names for TREM2 Antibody (2B5) - BSA Free
PLOSL2
TREM2
TREM-2
Trem2a
Trem2b
Trem2c
TREM-2triggering receptor expressed on myeloid cells 2a
Triggering receptor expressed on monocytes 2
triggering receptor expressed on myeloid cells 2
Background
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
Limitations
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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