Recombinant Human TREM-1 Protein(His Tag) (PDMH100168)

For research use only.
Synonyms | Triggering receptor expressed on myeloid cells, sTREM, OTTMUSP, TREM1, CD354, TREM-1, OTTMUSP00000018206, sTREM-1, TREM 1, Triggering receptor expressed on monocytes 1, Triggering receptor TREM 1, Triggering receptor TREM1, Triggering receptor expressed on myeloid cells 1 |
Species | Human |
Expression Host | Mammalian |
Sequence | Met1-Arg200 |
Accession | Q9NP99 |
Calculated Molecular Weight | 21.9 kDa |
Observed Molecular Weight | 30-40 kDa |
Tag | C-His |
Bio-activity | Not validated for activity |
Purity | > 95% as determined by reducing SDS-PAGE. |
Endotoxin | < 1.0 EU/mg of the protein as determined by the LAL method |
Storage | Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months. |
Shipping | This product is provided as lyophilized powder which is shipped with ice packs. |
Formulation | Lyophilized from a 0.2 μm filtered solution in PBS with 5% Trehalose and 5% Mannitol. |
Reconstitution | It is recommended that sterile water be added to the vial to prepare a stock solution of 0.5 mg/mL. Concentration is measured by UV-Vis |
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. |
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