Anti-TREM-1 Antibody (Mouse Monoclonal antibody) General Information
Reacts with: Human
Recombinant Human TREM1 protein (Catalog#10511-H03H)
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.
Monoclonal Mouse IgG2b Clone #6E8G4D4
0.2 μm filtered solution in PBS
This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
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 -80℃. Preservative-Free. Avoid repeated freeze-thaw cycles.
Please Note: Optimal concentrations/dilutions should be determined by the end user.
Anti-TREM-1 Antibody: Alternative Names
Anti-CD354 Antibody; Anti-TREM-1 Antibody
TREM-1 Background Information
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.