Mouse TREM2 Antibody Summary
Leu19-Pro168
Accession # Q99NH8
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Reconstitution Calculator
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: TREM2
TREM2 (Triggering Receptor Expressed on Myeloid cells-2) is a 35 kDa molecular weight type I transmembrane member of the TREM family and Ig superfamily. Mature human TREM2 consists of a 156 amino acid (aa) extracellular domain (ECD) with one V-type Ig-like domain, a 21 aa transmembrane (TM) domain, and a 35 aa cytoplasmic tail. Within the ECD, human TREM2 shares 73% and 74% aa sequence identity with mouse and rat TREM2, respectively. Two closely related transcripts were reported in mouse and designated TREM2a and TREM2b. Soluble forms of the TREM2 ECD are generated by alternative splicing or proteolytic cleavage, and the cytoplasmic domain can be liberated by gamma-Secretase mediated intramembrane cleavage. It is a pattern recognition receptor that binds anionic ligands. A positively charged lysine within the transmembrane segment allows association with the signal adapter protein, DAP12 to deliver an activating signal that plays a role in both innate and adaptive immune responses, including inhibition of macrophage activation. TREM2 is expressed on macrophages, immature myeloid dendritic cells, osteoclasts, microglia, and adipocytes. It promotes the differentiation and function of osteoclasts, the production of inflammatory cytokines by adipocytes, insulin resistance, and the phagocytic clearance of bacteria. In the CNS, TREM2 binds to ApoE, ApoA1, and ApoB and mediates the clearance of apoptotic neurons, amyloid plaques, and cell debris following demyelination. TREM2 also interacts with and modifies signaling through Plexin A1 on dendritic cells and osteoclasts. Mutations in TREM2 or DAP12 are associated with the development of Alzheimer's disease and Nasu-Hakola disease (NHD/PLOSL) which is characterized by presenile dementia and bone cysts. Soluble TREM2 is elevated in cerebrospinal fluid of patients with active multiple sclerosis (MS), and TREM2 blockade exacerbates disease symptoms in the experimental EAE model of MS.
Product Datasheets
Citations for Mouse TREM2 Antibody
R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.
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Citations: Showing 1 - 10
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The cholesteryl ester transfer protein (CETP) raises cholesterol levels in the brain
Authors: Felix Oestereich, Noosha Yousefpour, Ethan Yang, Jasmine Phénix, Zari Saadati Nezhad, Albert Nitu et al.
Journal of Lipid Research
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MS4A4A modifies the risk of Alzheimer disease by regulating lipid metabolism and immune response in a unique microglia state
Authors: SF You, L Brase, F Filipello, AK Iyer, J Del-Aguila, J He, R D'Oliveira, J Budde, J Norton, J Gentsch, NM Dräger, SM Sattler, M Kampmann, L Piccio, JC Morris, RJ Perrin, E McDade, Dominantly, SM Paul, AG Cashikar, BA Benitez, O Harari, CM Karch
medRxiv : the preprint server for health sciences, 2023-02-08;0(0):.
Species: Mouse
Sample Types: Cell Culture Supernates
Applications: ELISA Capture -
Trem2 Y38C mutation and loss of Trem2 impairs neuronal synapses in adult mice
Authors: VS Jadhav, PBC Lin, T Pennington, GV Di Prisco, AJ Jannu, G Xu, M Moutinho, J Zhang, BK Atwood, SS Puntambeka, SJ Bissel, AL Oblak, GE Landreth, BT Lamb
Mol Neurodegener, 2020-10-28;15(1):62.
Species: Mouse
Sample Types: Cell Lysates
Applications: ELISA Capture -
TREM2 shedding by cleavage at the H157-S158 bond is accelerated for the Alzheimer's disease-associated H157Y variant
Authors: P Thornton, J Sevalle, MJ Deery, G Fraser, Y Zhou, S Ståhl, EH Franssen, RB Dodd, S Qamar, B Gomez Pere, LS Nicol, S Eketjäll, J Revell, C Jones, A Billinton, PH St George-, I Chessell, DC Crowther
EMBO Mol Med, 2017-10-01;0(0):.
Species: Mouse
Sample Types: Cell Lysates
Applications: Western Blot -
The FTD-like syndrome causing TREM2 T66M mutation impairs microglia function, brain perfusion, and glucose metabolism
Authors: G Kleinberge, M Brendel, E Mracsko, B Wefers, L Groeneweg, X Xiang, C Focke, M Deu beta ing, M Suárez-Cal, F Mazaheri, S Parhizkar, N Pettkus, W Wurst, R Feederle, P Bartenstei, T Mueggler, T Arzberger, I Knuesel, A Rominger, C Haass
EMBO J., 2017-05-30;0(0):.
Species: Mouse
Sample Types: CSF
Applications: ELISA Development -
Increase of TREM2 during Aging of an Alzheimer's Disease Mouse Model Is Paralleled by Microglial Activation and Amyloidosis
Authors: M Brendel, G Kleinberge, F Probst, A Jaworska, F Overhoff, T Blume, NL Albert, J Carlsen, S Lindner, FJ Gildehaus, L Ozmen, M Suárez-Cal, P Bartenstei, K Baumann, M Ewers, J Herms, C Haass, A Rominger
Front Aging Neurosci, 2017-01-31;9(0):8.
Species: Mouse
Sample Types: Tissue Homogenates
Applications: ELISA Development (Detection) -
Osteoprotection by semaphorin 3A.
Authors: Hayashi M, Nakashima T, Taniguchi M, Kodama T, Kumanogoh A, Takayanagi H
Nature, 2012-05-03;485(7396):69-74.
Species: Mouse
Sample Types: Cell Lysates
Applications: Western Blot -
Lentiviral vector-mediated overexpression of mutant ataxin-7 recapitulates SCA7 pathology and promotes accumulation of the FUS/TLS and MBNL1 RNA-binding proteins
Authors: Sandro Alves, Thibaut Marais, Maria-Grazia Biferi, Denis Furling, Martina Marinello, Khalid El Hachimi et al.
Molecular Neurodegeneration
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Uncovering Disease Mechanisms in a Novel Mouse Model Expressing Humanized APOE epsilon 4 and Trem2*R47H
Authors: Kotredes KP, Oblak A, Pandey RS Et al.
Frontiers in aging neuroscience
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Trem2 H157Y increases soluble TREM2 production and reduces amyloid pathology
Authors: Wenhui Qiao, Yixing Chen, Jun Zhong, Benjamin J. Madden, Cristine M. Charlesworth, Yuka A. Martens et al.
Molecular Neurodegeneration
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