WB, IF-IC, FC-FP
H
Endogenous
28
Rabbit IgG
#Q9NZC2
54209
Product Information
Product Usage Information
This product is the carrier-free version of product #91068. All data were generated using the same antibody clone in the standard formulation which contains BSA and glycerol.
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN, or CUT&Tag assays. If you require a carrier-free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.
Formulation
Supplied in 1X PBS, BSA and Azide Free.
For standard formulation of this product see product #91068.
Storage
Specificity / Sensitivity
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu221 of human TREM2 protein.
Background
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 microglial 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).
- Colonna, M. (2003) Nat Rev Immunol 3, 445-53.
- Jonsson, T. et al. (2013) N Engl J Med 368, 107-16.
- Boutajangout, A. and Wisniewski, T. (2013) Int J Cell Biol 2013, 576383.
- Wang, Y. et al. (2015) Cell 160, 1061-71.
- Melchior, B. et al. (2010) ASN Neuro 2, e00037.
- Klünemann, H.H. et al. (2005) Neurology 64, 1502-7.
- Thornton, P. et al. (2017) EMBO Mol Med 9, 1366-1378.
- Schlepckow, K. et al. (2017) EMBO Mol Med 9, 1356-1365.
Species Reactivity
Species reactivity is determined by testing in at least one approved application (e.g., western blot).
Applications Key
WB: Western Blotting IF-IC: Immunofluorescence (Immunocytochemistry) FC-FP: Flow Cytometry (Fixed/Permeabilized)
Cross-Reactivity Key
H: human M: mouse R: rat Hm: hamster Mk: monkey Vir: virus Mi: mink C: chicken Dm: D. melanogaster X: Xenopus Z: zebrafish B: bovine Dg: dog Pg: pig Sc: S. cerevisiae Ce: C. elegans Hr: horse GP: Guinea Pig Rab: rabbit All: all species expected
Trademarks and Patents
Limited Uses
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