Rat monoclonal [L5-B8.2A12.3A12] antibody to TREM1.
Spezifität
This antibody recognises mouse triggering receptor expressed on myeloid cells 1 (TREM-1), a 30kD member of the immunoglobulin superfamily expressed on neutrophils and a subset of monocytes. TREM-1 is involved in the microbial inflammatory response. It acts in conjunction with the adaptor protein DAP12 to activate neutrophils and monocytes, leading to the secretion of pro-inflammatory mediators and enhancement of the inflammatory response. Microbial infection also induces the release of soluble form of TREM-1 from monocytes, which is reported to act as an inhibitor of TREM-1. TREM-1 mediates the septic shock pathway, and blocking TREM-1 has been reported to reduce inflammation and increase survival in certain models of bacterial infection.
Anwendungen
WB, Flow Cytometry, IHC-Fr, IF
Verdünnungen
Flow Cytometry: 1:25 - 1:100, Use 10µl of the suggested working dilution to label 1x106 cells in 100µl.
Reaktivität
Mouse
Immunogen
Mouse TREM-1 Fc fusion protein.
Wirt
Rat
Klonalität
Monoclonal
Klon
L5-B8.2A12.3A12
Isotyp
IgG2a
Konjugat
Unconjugated
Reinigung
Protein G affinity chromatography of tissue culture supernatant.
Konzentration
1 mg/ml
Produktform
Liquid
Formulierung
Supplied in Phosphate Buffered Saline with 0.09% Sodium Azide.
Lagerung
Shipped at ambient temperature. Upon delivery aliquot and store at -20°C. When thawed, aliquot the sample as needed. Short term (up to 4 weeks): store at 4°C. Long term: store at -20°C. Avoid freeze / thaw cycles. Storage in frost free freezers is not recommended.
Allgemeine Hinweise
Rat anti Mouse Trem-1 antibody, clone L5-B8.2A12.3A12 recognizes mouse triggering receptor expressed on myeloid cells 1 (TREM-1), a 30kD member of the immunoglobulin superfamily expressed on neutrophils and a subset of monocytes. TREM-1 is involved in the microbial inflammatory response. It acts in conjunction with the adaptor protein DAP12 to activate neutrophils and monocytes, leading to the secretion of pro-inflammatory mediators and enhancement of the inflammatory response. Microbial infection also induces the release of soluble form of TREM-1 from monocytes, which is reported to act as an inhibitor of TREM-1. TREM-1 mediates the septic shock pathway, and blocking TREM-1 has been reported to reduce inflammation and increase survival in certain models of bacterial infection.