Overview
Alomone Labs N-Formyl-Met-Leu-Phe activates Ca2+ transients in differentiated HL-60 cells.Cells were loaded with Fluo-3 AM. Changes in intracellular Ca2+ were detected via changes in Fluo-3 emission following application (indicated by arrow) of 1 µM N-Formyl-Met-Leu-Phe (#GPF-100), (green) compared to control (black, saline perfusion).
Chemotactic factors from both Gram-positive and Gram-negative bacteria are short peptides with N-formyl methionine at the N-terminus (extensively reviewed in reference 1). These peptides are released from bacteria during infection and activate formyl peptide receptors (FPR), members of the G-protein coupled receptor (GPCR) superfamily. In humans, the FPR family consists mainly of three receptors, FPR1, FPR2/ALX (formerly FPRL1), and FPR3 (formerly FPRL2) which all couple to the Gi subtype of G-proteins and ultimately lead to the activation of phospholipase C and intracellular Ca2+ increase1,2.
N-Formyl-Met-Leu-Phe is a selective and potent agonist of the Formyl peptide receptor (FPR1)3.
In human polymorphonuclear leukocytes N-formyl-met-leu-phe activates p38 by a process involving phosphatidylinositol 3-kinase, protein kinase C, and calcium4. N-Formyl-Met-Leu-Phe increased in a dose-dependent manner (0.1 nM – 1 µM) the adherence of neutrophils to vascular endothelial cells which is the initial event in the migration of neutrophils through blood vessel walls to tissue sites of inflammation5.
FPR1 receptor
