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Recombinant Human TREM1 Protein (His & Fc Tag)

Uniprot : Q38L15
  • Cat.No.:PKSH031561

  • Expression host: HEK293 Cells

To Purchase PKSH031561

Size:
  • 100μg
Price: $732
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Description

Synonyms Triggering Receptor Expressed on Myeloid Cells 1;TREM-1;Triggering Receptor Expressed on Monocytes 1;CD354;TREM1
Species Human
Expression_host HEK293 Cells
Sequence Met 1-Arg 200
Accession NP_061113.1
Mol_Mass 48.3 kDa
AP_Mol_Mass 60-65 kDa
Tag C-His-Fc
Bio_Activity Not validated for activity

Properties

Purity > 97 % as determined by reducing SDS-PAGE.
Endotoxin level < 1.0 EU per μg 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 sterile PBS, pH 7.4
Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization.
Please refer to the specific buffer information in the printed manual.
Reconstitution Please refer to the printed manual for detailed information.

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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