KLRG1 Monoclonal Antibody (2F1), PE, eBioscience™, Invitrogen™

Beschreibung

Description: This 2F1 monoclonal antibody reacts with the mouse Killer cell Lectin-like Receptor G1 (KLRG1), also known as Mast cell Function-associated Antigen (MAFA). KLRG1 is a homodimer of glycosylated 30-38 kDa subunits and contains a cytoplasmic motif similar to the immunoreceptor tyrosine-based inhibitory motif (ITIM). Rat MAFA was identified as an antigen specific to rat mast cells; however, the expression of mouse KLRG1/MAFA using 2F1 has not been detected on the surface of mouse mast cell lines, bone marrow-derived mast cells, or peritoneal mast cells. This antigen is expressed on approximately one-third of mouse NK cells and a subset of T cells. MHC class I molecules regulate KLRG1 via interactions with class I-specific inhibitory Ly49 molecules and SHP-1 signaling. Although KLRG1 and Ly49 are both lectin-like inhibitory receptors that are regulated by class I MHC expression, the effects of this on cell surface expression of these molecules are opposing, and the underlying regulatory mechanisms distinct. Applications Reported: This 2F1 antibody has been reported for use in flow cytometric analysis. Applications Tested: This 2F1 antibody has been tested by flow cytometric analysis of mouse splenocytes. This can be used at less than or equal to 0.25 μg per test. A test is defined as the amount (μg) of antibody that will stain a cell sample in a final volume of 100 μL.

KLRG1 (Killer cell lectin-like receptor G1, MAFA, 2F1-Ag) is a homodimeric member of the lectin-like type 2 transmembrane receptor family whose members contain characteristic immunoreceptor tyrosine-based inhibitory motifs (ITIMs) in their cytoplasmic domains. These ITIMs interact with the SH2 domains of protein phosphatases such as SHP-1. KLRG1 is an inhibitory receptor that is expressed on natural killer (NK) cells and certain T cells. NK cells are involved in the lysis of tumor cells and virus-infected cells, and mediate humoral and cell-mediated immune responses.