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TREM1 Antibody, Mouse MAb

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TREM1Antibody Product Information
Immunogen:Recombinant Human TREM1 protein (Catalog#10511-H03H)
Clone ID:6E8G4D4
Ig Type:Mouse IgG2b
Concentration:
Formulation:0.2 μm filtered solution in PBS with 5% trehalose
Preparation: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 TREM1 (rh TREM1; Catalog#10511-H03H; NP_061113.1; Met 1-Arg 200). The IgG fraction of the cell culture supernatant was purified by Protein A affinity chromatography.
TREM1Antibody Usage Guide
Specificity:Human TREM1
No cross-reactivity with Human cell lysate (293 cell line) in WB and ELISA.
Application:ELISA

ELISA: 0.5-1 μg/mL

This antibody can be used at 0.5-1 μg/mL with the appropriate secondary reagents to detect Human TREM1. The detection limit for Human TREM1 is 0.078 ng/well.

Storage:This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -70℃. Preservative-Free.
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.
Background

TREM1 (triggering receptor expressed on myeloid cells) is a type I  transmembrane protein with a single Ig-like domain, and is selectively expressed on blood neutrophils and a subset of monocytes. As a member of the growing family of receptors related to NK cell receptors, TREM1 activates downstream signaling events with the help of an adapter protein called DAP12. Expression of TREM1 is up-regulated by bacterial LPS, a ligand for TLR4, as well as lipoteichoic acid. Although its natural ligand has not been identified, engagement of TREM1 with agonist mAbs triggers secretion of the proinflammatory cytokines TNF-α and IL-1β, as well as chemokines such as IL-8 and monocyte chemoattractant protein (MCP)-1. Intracellularly, TREM1 induces Ca2+ mobilization and tyrosine phosphorylation of extracellular signal-related kinase 1 (ERK1), ERK2 and phospholipase C-γ. In an animal model of LPS-induced septic shock, blockade of TREM1 signaling inhibited hyperresponsiveness and death. Thus, it has been demonstrated that TREM1 performs a critical function in immune responses involved in host defense against microbial challenges, and is suggested to be a potential therapeutic target for septic shock.

References
  • Bouchon, A. et al., 2000, J. Immunol. 164: 4991-4995.
  • Bouchon, A. et al., 2001, Nature. 410: 1103-1107.
  • Bleharski, J.R. et al., 2003, J. Immunol. 170: 3812-3818.
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