N-Formyl-Met-Leu-Phe (Synonyms: Chemotactic Peptide, fMLF, fMLP, NSC 350593) |
Katalog-Nr.GC16673 |
N-Formyl-Met-Leu-Phe (fMLP; N-Formyl-MLF) ist ein chemotaktisches Peptid und ein spezifischer Ligand des N-Formyl-Peptid-Rezeptors (FPR).
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Cas No.: 59880-97-6
Sample solution is provided at 25 µL, 10mM.
N-Formyl-Met-Leu-Phe (fMLP) is an endogenous chemotactic peptide and an agonist of formyl peptide receptor 1 (FPR1) with a Ki value of 38 nM[1]. N-Formyl-Met-Leu-Phe activates various functions of neutrophils and monocytes by binding to G protein-coupled receptors, causing cell polarization, the production of reactive oxygen species, and the release of arachidonic acid metabolites. production and release of lysosomal enzymes[2]. N-Formyl-Met-Leu-Phe is a bacterial-derived peptide that synergizes with lipopolysaccharide to induce inflammatory responses through multiple signaling pathways[3].
In vitro, N-Formyl-Met-Leu-Phe (1μM) stimulated human osteoblasts for 1 hour, significantly increased the activities of intracellular PLC and PLD, increased the expression levels of Runx2 and COX2, and promoted the differentiation of cells into osteoblasts[4]. N-Formyl-Met-Leu-Phe (100nM) treated U937 cells, which enhanced intracellular Ca2+ signal transduction and hyperpolarized the cells[5]. N-Formyl-Met-Leu-Phe (10μM/ml) treated human neutrophils and stimulated the production of superoxide anions [6].
In vivo, N-Formyl-Met-Leu-Phe (1μM) treated newly fertilized zebrafish embryos and promoted bone development; N-Formyl-Met-Leu-Phe (50μM) treated rabbits with skull defects and promoted bone reconstruction[4]. N-Formyl-Met-Leu-Phe (1μM) treatment of mice increased leukocyte infiltration in the air sacs and aggravated air sac inflammation [7].
References:
[1]Mills J S, Miettinen H M, Cummings D, et al. Characterization of the binding site on the formyl peptide receptor using three receptor mutants and analogs of Met-Leu-Phe and Met-Met-Trp-Leu-Leu[J]. Journal of Biological Chemistry, 2000, 275(50): 39012-39017.
[2]Panaro M A, Mitolo V. Cellular responses to FMLP challenging: a mini-review[J]. Immunopharmacology and immunotoxicology, 1999, 21(3): 397-419.
[3]Chen L Y, Pan W W, Chen M, et al. Synergistic induction of inflammation by bacterial products lipopolysaccharide and fMLP: an important microbial pathogenic mechanism[J]. The Journal of Immunology, 2009, 182(4): 2518-2524.
[4]Shin M K, Jang Y H, Yoo H J, et al. N-formyl-methionyl-leucyl-phenylalanine (fMLP) promotes osteoblast differentiation via the N-formyl peptide receptor 1-mediated signaling pathway in human mesenchymal stem cells from bone marrow[J]. Journal of Biological Chemistry, 2011, 286(19): 17133-17143.
[5]Penna A, Stutzin A. KCa3. 1-dependent hyperpolarization enhances intracellular Ca2+ signaling induced by fMLF in differentiated U937 cells[J]. PLoS One, 2015, 10(9): e0139243.
[6]Chniguir A, Pintard C, Liu D, et al. Eugenol prevents fMLF-induced superoxide anion production in human neutrophils by inhibiting ERK1/2 signaling pathway and p47phox phosphorylation[J]. Scientific reports, 2019, 9(1): 18540.
[7]Cui Y, Hou X, Chen J, et al. Sesamin inhibits bacterial formylpeptide-induced inflammatory responses in a murine air-pouch model and in THP-1 human monocytes[J]. The Journal of nutrition, 2010, 140(2): 377-381.
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