Anti-TREM1 Antibody [L5-B8.2A12.3A12] - BSA and Azide free (A280852)

Anti-TREM1 Antibody [L5-B8.2A12.3A12] - BSA and Azide free

Rat monoclonal [L5-B8.2A12.3A12] antibody to TREM1.

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.

IHC-Fr, WB, Flow Cytometry, Functional Assays, IF

Flow Cytometry: 1:25 - 1:100, Use 10µl of the suggested working dilution to label 1x10⁶ cells in 100µl.

Mouse

Mouse TREM-1 Fc fusion protein.

Rat

Monoclonal

L5-B8.2A12.3A12

IgG2a

1 mg/ml

Liquid

Supplied in Phosphate Buffered Saline.

Store undiluted at -20°C only. Storage in frost free freezers is not recommended. Avoid freeze-thaw cycles. Should this product contain a precipitate we recommend microcentrifugation before use.

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.

CD354, TREM-1, Triggering receptor expressed on monocytes 1, Triggering receptor expressed on myeloid cells 1