Rat monoclonal [L5-B8.2A12.3A12] antibody to TREM1 (PE).
Specificità
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.
Applicazioni
Flow Cytometry
Diluizioni consigliate
Flow Cytometry: Neat, Use 10µl of the suggested working dilution to label 1x106 cells in 100µl.
Reattività
Mouse
Immunogeno
Mouse TREM-1 Fc fusion protein.
Specie ospite
Rat
Clonalità
Monoclonal
Clona ID
L5-B8.2A12.3A12
Isotipo
IgG2a
Coniugare
PE
Excitation: 565nm, Emission: 578nm
Purificazione
Protein G affinity chromatography of tissue culture supernatant.
Concentrazione
Reconstitution dependent.
Forma del prodotto
Lyophilized
Ricostituzione
Reconstitute with 1 ml of distilled water.
Formulazione
Supplied in Phosphate Buffered Saline with 1% BSA, 5% Sucrose, and 0.09% Sodium Azide.
Conservazione
Store undiluted at 4°C. Do not freeze! This product is photosensitive and should be protected from light. Should this product contain a precipitate we recommend microcentrifugation before use.
Note generali
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.