This IgG mouse monoclonal was generated against human neutrophil N-formyl peptide receptor, NFPRa and recognizes FPR1 and FPR2.
Formyl peptide receptors (FPR) are a family of G-protein-coupled receptors of mammalian phagocytic cells and are involved in antibacterial host defense and inflammation. Activating these receptors can mediate neutrophil chemotaxis, production of reactive oxygen species and stimulate degranulation of neutrophils.
Also available: Anti-FPR1 [NFPRb] Antibody.
From the laboratory of Algirdas J. Jesaitis, PhD, Montana State University.
Part of The Investigator's Annexe program.
|Specificity:||Neutrophil and recombinant FPR1 and FPR2|
|Immunogen:||Expressed and purified a hexa-histidine-tagged recombinant FPR1 (rHis-FPR1) in Spodoptera frugiperda(Sf9) cells|
|Epitope:||Cytoplasmic c-terminal tail residues of FPR1 305-GQDFRERLI-313 and of FRP2 306-GQDFRERLI-314|
|Buffer:||0.1M Sodium Phosphate, pH 7.4, 0.15M NaCl, 0.05% (w/v) Sodium Azide|
|Tested Applications:||WB, IF, IP (1:1000-4000), (2 -0.5?g/ml; depending on detection system)|
Recognition of FPR1 and FPR2 in unstimulated neutrophil homogenates and membranes
SDS-PAGE-separated and immunoblotted whole cell lysates (L) and salt-washed membranes (M) from N2 cavitates of unstimulated neutrophils, as described under Experimental Procedures, were developed with the NFPRb (left two lanes) and NFPRa (right two lanes) primary mAbs and visualized by infrared fluorescence scanning with a LI-COR Odyssey scanner. Each lane contains 2 × 105 cell equivalents. The broadly staining band between Mr ?50,000 and 65,000 (also known as 60K) is putatively FPR1 and is recognized by both mAbs. The band between Mr ?41,000 and 50,000 (also known as 45K) comigrates with FPR2 and is only recognized by NFPRa. The more intense bands at ?30,000 and ?36,000 are soluble cytosolic species and are lost in the particulate fraction.
Adapted from: Maaty WS, et al., J Biol Chem. 2013 Sep 20;288(38):27042-58.
If you publish research with this product, please let us know so we can cite your paper.