Recombinant Cynomolgus Monkey TREM2 Fc Chimera Protein, CF

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Recombinant Cynomolgus Monkey TREM2 Fc Chimera Protein, CF (Catalog # 10840-T2) binds fluorescein-conjugated E. coli Bioparticles with an ED50 of 20.0-120 ng/mL.
2 μg/lane of Recombinant Cynomolgus Monkey TREM2 Fc Chimera (Catalog # 10840-T2) was resolved with SDS-PAGE under reducing (R) and non-reducing (NR) conditions and visualized by Coomassie® Blue staining, showing ...read more

Product Details

Summary
Reactivity Pm-CmSpecies Glossary
Applications Bioactivity
Format
Carrier-Free

Order Details

Recombinant Cynomolgus Monkey TREM2 Fc Chimera Protein, CF Summary

Details of Functionality
Measured by its ability to bind fluorescein-conjugated E. coli Bioparticles. The ED50 for this effect is 20.0-120 ng/mL.
Source
Human embryonic kidney cell, HEK293-derived cynomolgus monkey TREM2 protein
Cynomolgus Monkey TREM2
(His19-Ser174)
Accession # XP_005553122.1
IEGRMD Human IgG1
(Pro100-Lys330)
N-terminusC-terminus
Accession #
N-terminal Sequence
His19
Structure / Form
Disulfide-linked homodimer
Protein/Peptide Type
Recombinant Proteins
Purity
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Endotoxin Note
<0.10 EU per 1 μg of the protein by the LAL method.

Applications/Dilutions

Dilutions
  • Bioactivity
Theoretical MW
44 kDa.
Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
SDS-PAGE
55-65 kDa, under reducing conditions

Packaging, Storage & Formulations

Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 12 months from date of receipt, -20 to -70 °C as supplied.
  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.
  • 3 months, -20 to -70 °C under sterile conditions after reconstitution.
Buffer
Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose.
Purity
>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
Reconstitution Instructions
Reconstitute at 500 μg/mL in PBS.

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for Recombinant Cynomolgus Monkey TREM2 Fc Chimera Protein, CF

  • 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 type I transmembrane member of the TREM subfamily within the much larger Ig superfamily. In humans, there are 7 TREM and TREM-like receptors which play important roles in the regulation of both innate and adaptive immune response (1). Mature cynomologus TREM2 consists of an extracellular domain (ECD) with one V-type Ig-like domain, a transmembrane domain with a conserved positively-charged lysine residue, and a short cytoplasmic tail (1). The ECD of Cynomologus TREM2 shares 97% amino acid identity with human TREM2. TREM2 is expressed on macrophages, immature myeloid dendritic cells, osteoclasts, microglia, and adipocytes (2-6). It promotes the differentiation and function of osteoclasts, the production of inflammatory cytokines by adipocytes, insulin resistance, and the phagocytic clearance of bacteria (6-8). TREM2 associates with the signaling adapter protein DAP12, both preferentially expressed in microglia, to modulate cytokine production (2). Additionally in the CNS, TREM2 binds to ApoE, ApoA1, and ApoB and mediates the clearance of apoptotic neurons, amyloid plaques, and cell debris following demyelination (3-5, 9). TREM2 also interacts with and modifies the signaling of Plexin A1 on dendritic cells and osteoclasts (10). 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 (11, 12). 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 (13, 14).
  1. Klesney-Tait, J. et al. (2006) Nat Immunol 7:1266.
  2. Turnbull, I.R. et al. (2006) J. Immunol. 177:3520.
  3. Takahashi, K. et al. (2005) J. Exp. Med. 201:647.
  4. Atagi, Y. et al. (2015) J. Biol. Chem. 290:26043.
  5. Wang, Y. et al. (2016) J. Exp. Med. 213:667.
  6. Cella, M. et al. (2003) J. Exp. Med. 198:645.
  7. Park, M. et al. (2015) Diabetes 64:117.
  8. N'Diaye, E-N. et al. (2009) J. Cell Biol. 184:215.
  9. Poliani, P.L. et al. (2015) J. Clin. Invest. 125:2161.
  10. Takegahara, N. et al. (2006) Nat. Cell Biol. 8:615.
  11. Colonna, M. and Y. Wang (2016) Nat. Rev. Neurosci. 17:201.
  12. Paloneva, J. et al. (2002) Am. J. Hum. Genet. 71:656.
  13. Piccio, L. et al. (2008) Brain 131:3081.
  14. Piccio, L. et al. (2007) Eur. J. Immunol. 37:1290.

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