Anti-TREM1 antibody

Cat.#: 141430

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Product Information

  • Product Name
    Anti-TREM1 antibody
  • Documents
  • Description
    Mouse Monoclonal to Human TREM1
  • Tested applications
    FCM
  • Species reactivity
    Human TREM-1 / TREM1
  • Alternative names
    TREM1 antibody; TREM-1 antibody; CD354 antibody; TREM-1 antibody
  • Immunogen
  • Isotype
    Mouse IgG1
  • 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 TREM-1 / TREM1 and conjugated with PE under optimum conditions, the unreacted PE was removed.
  • Clonality
    Monoclonal
  • Formulation
    Aqueous solution containing 0.5% BSA and 0.09% sodium azide
  • Storage instructions
    This antibody is stable for 12 months from date of receipt when stored at 2℃-8℃. Protected from prolonged exposure to light. Do not freeze !
    Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.
  • Applications
    FCM
  • Validations

    Human TREM-1/TREM1 Flow Cytometry (FC) 15076

    Human TREM-1/TREM1 Flow Cytometry (FC) 15076

  • 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.

Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"