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Chemical Compound Review

fMet-Leu-Phe     (2S)-2-[[(2S)-2-[[(2S)-2- formamido-4...

Synonyms: fMetLeuPhe, FMLP, fMLF, F-Met-leu-phe, CHEMBL267179, ...
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Disease relevance of Formyl met leu phe


High impact information on Formyl met leu phe

  • A similar conclusion has been applied to explain the actions of formyl-Met-Leu-Phe on neutrophils, and it may be that receptors that couple through intrinsic tyrosine kinases or through G proteins stimulate the same step in 3-phosphorylated inositol lipid metabolism [6].
  • The loss of IL-1 binding capacity caused by FMLP was determined by a reduction in receptor number with no change in their affinity [7].
  • N-t-Boc-Met-Leu-Phe, an antagonist for the FMLP receptor, inhibited the loss of IL-1 binding capacity induced by FMLP [7].
  • In response to formyl-Met-Leu-Phe (fMLP) receptor stimulation, beta-arrestin Ral-GDS protein complexes dissociate and Ral-GDS translocates with beta-arrestin from the cytosol to the plasma membrane, resulting in the Ras-independent activation of the Ral effector pathway required for cytoskeletal rearrangement [8].
  • The analysis of biological effects of TPO on PMN demonstrated that TPO, at concentrations of 1-10 ng/ml, primes the response of PMN to n-formyl-met-leu-phe (FMLP) by inducing an early oxidative burst [9].

Chemical compound and disease context of Formyl met leu phe


Biological context of Formyl met leu phe

  • Dose-response analysis revealed that maximal reduction of IL-1 binding was reached at FMLP concentrations that were also optimal for chemotaxis (50% effective dose = 5 x 10(-9) M) [7].
  • In studies of Ab 1-15 effects on membrane-related second messenger pathways, Ab 1-15 augmented both FMLP- and isoproterenol-induced intracellular cAMP accumulation, whereas alpha-chymotrypsin decreased PMN cAMP response to these stimuli [15].
  • We studied the time course of change in F-actin content, F-actin distribution, and cell shape after fMLP stimulation [16].
  • Out of a large panel of naturally occurring humoral factors tested, only GM-CSF itself, tumor necrosis factor, and formyl-Met-Leu-Phe were found to down-regulate neutrophil GM-CSF receptor expression after a 2-hr exposure at biologically active concentrations (95% +/- 1%, 34% +/- 5%, 48% +/- 8% receptor down-regulation, respectively) [17].
  • High and intermediate doses of FMLP caused a dramatic but transient decrease in blood pressure and an increase in respiratory rate [1].

Anatomical context of Formyl met leu phe


Associations of Formyl met leu phe with other chemical compounds

  • Although the initial acidification following fMLP was abrogated by 2-deoxy-D-glucose in both GM-CSFrh-pretreated and GM-CSFrh-untreated granulocytes, retardation of the subsequent phase of alkalinization was observed in GM-CSFrh-primed cells even after inhibition of both glycolytic and mitochondrial metabolism [22].
  • These results suggest that PLD plays an important role in fMLP stimulation of both N-acetyl-beta-glucosaminidase release and O2- generation in the primed neutrophils, but that a PLD-independent pathway plays the primary role in O2- generation by the nonprimed neutrophils [23].
  • Selective Localization of Recognition Complexes for Leukotriene B4 and Formyl-Met-Leu-Phe within Lipid Raft Microdomains of Human Polymorphonuclear Neutrophils [24].
  • A similar pretreatment with PT inhibited thrombin-induced histamine release from BMMC and N-formyl-L-methionyl-L-leucyl-L-phenylalanine-induced histamine release from human basophils in a similar dose-dependent fashion [25].
  • By use of a recently described and specific inhibitor of cytosolic PLA(2)-alpha (group IV PLA(2)alpha), we show that this enzyme produces virtually all of the arachidonic acid used for the biosynthesis of leukotriene B(4) in fMLP- and opsonized zymosan-stimulated neutrophils, the major eicosanoid produced by these pro-inflammatory cells [26].

Gene context of Formyl met leu phe

  • In addition, formyl-Met-Leu-Phe (a FPR ligand), Trp-Lys-Tyr-Met-Val-Met, Hp(2-20) peptide, and F2L (three FPRL2 ligands) inhibited LPS-induced IL-12 production in DCs [27].
  • Preincubation with IL-8, MGSA, or ENA-78 enhanced the ability of neutrophils to generate O-2 following stimulation with the bacterial peptide formyl-Met-Leu-Phe [28].
  • In formyl-Met-Leu-Phe-stimulated cells, PLD activity as assessed by phosphatidylethanol formation was also associated with both the plasma membrane and endomembranes [29].
  • This is in contrast to other neutrophil agonists such as fMLP, interleukin (IL)-8, or GM-CSF, which stimulate multiple MAPK pathways [30].
  • Ligation of CGM6 or NCA90 alone did not cause activation of the neutrophil in any of the assays used and did not cause priming of fMLP-induced oxidant production even when a secondary cross-linking reagent was used [31].

Analytical, diagnostic and therapeutic context of Formyl met leu phe


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  4. Altered signal pathway in granulocytes from patients with hypercholesterolemia. Paragh, G., Kovács, E., Seres, I., Keresztes, T., Balogh, Z., Szabó, J., Teichmann, F., Fóris, G. J. Lipid Res. (1999) [Pubmed]
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  8. Beta-arrestins regulate a Ral-GDS Ral effector pathway that mediates cytoskeletal reorganization. Bhattacharya, M., Anborgh, P.H., Babwah, A.V., Dale, L.B., Dobransky, T., Benovic, J.L., Feldman, R.D., Verdi, J.M., Rylett, R.J., Ferguson, S.S. Nat. Cell Biol. (2002) [Pubmed]
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  12. Activation of the respiratory burst in eosinophil leucocytes--a transduction sequence decoupled from cytosolic Ca2+ rise. Wymann, M.P., Kernen, P., Von Tscharner, V., Tai, P.C., Spry, C.J., Baggiolini, M. Eur. J. Clin. Invest. (1995) [Pubmed]
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  14. Neutrophil stimulating activity released by Staphylococcus-stimulated mononuclear leukocyte conditioned medium. Further characterization and partial purification. Ferrante, A., Bates, E.J., Nandoskar, M. J. Chromatogr. (1988) [Pubmed]
  15. Monoclonal antibody characterization of a chymotrypsin-like molecule on neutrophil membrane associated with cellular activation. King, C.H., Goralnik, C.H., Kleinhenz, P.J., Marino, J.A., Sedor, J.R., Mahmoud, A.A. J. Clin. Invest. (1987) [Pubmed]
  16. The kinetics of chemotactic peptide-induced change in F-actin content, F-actin distribution, and the shape of neutrophils. Howard, T.H., Oresajo, C.O. J. Cell Biol. (1985) [Pubmed]
  17. Regulation of surface expression of the granulocyte/macrophage colony-stimulating factor receptor in normal human myeloid cells. Cannistra, S.A., Groshek, P., Garlick, R., Miller, J., Griffin, J.D. Proc. Natl. Acad. Sci. U.S.A. (1990) [Pubmed]
  18. Modulation of human neutrophil effector functions by monoclonal antibodies against surface membrane molecules of 94,000 and 180,000 molecular weight. King, C.H., Peck, C.A., Haimes, C.S., Kazura, J.W., Spagnuolo, P.J., Sawyer, J.A., Olds, G.R., Mahmoud, A.A. Blood (1986) [Pubmed]
  19. Signal transduction and the regulation of actin conformation during myeloid maturation: studies in HL60 cells. Sham, R.L., Packman, C.H., Abboud, C.N., Lichtman, M.A. Blood (1991) [Pubmed]
  20. G-protein-coupled receptor signaling in Syk-deficient neutrophils and mast cells. Mócsai, A., Zhang, H., Jakus, Z., Kitaura, J., Kawakami, T., Lowell, C.A. Blood (2003) [Pubmed]
  21. Comparative study of eosinophil and neutrophil chemotaxis and enzyme release. Ogawa, H., Kunkel, S.L., Fantone, J.C., Ward, P.A. Am. J. Pathol. (1981) [Pubmed]
  22. Effects of recombinant human granulocyte-macrophage colony-stimulating factor on intracellular pH in mature granulocytes. Sullivan, R., Griffin, J.D., Wright, J., Melnick, D.A., Leavitt, J.L., Fredette, J.P., Horne, J.H., Lyman, C.A., Lazzari, K.G., Simons, E.R. Blood (1988) [Pubmed]
  23. The phosphatase inhibitor 2,3-diphosphoglycerate interferes with phospholipase D activation in rabbit peritoneal neutrophils. Kanaho, Y., Nakai, Y., Katoh, M., Nozawa, Y. J. Biol. Chem. (1993) [Pubmed]
  24. Selective Localization of Recognition Complexes for Leukotriene B4 and Formyl-Met-Leu-Phe within Lipid Raft Microdomains of Human Polymorphonuclear Neutrophils. Sitrin, R.G., Emery, S.L., Sassanella, T.M., Blackwood, R.A., Petty, H.R. J. Immunol. (2006) [Pubmed]
  25. Effects of ADP-ribosylation of GTP-binding protein by pertussis toxin on immunoglobulin E-dependent and -independent histamine release from mast cells and basophils. Saito, H., Okajima, F., Molski, T.F., Sha'afi, R.I., Ui, M., Ishizaka, T. J. Immunol. (1987) [Pubmed]
  26. Groups IV, V, and X phospholipases A2s in human neutrophils: role in eicosanoid production and gram-negative bacterial phospholipid hydrolysis. Degousee, N., Ghomashchi, F., Stefanski, E., Singer, A., Smart, B.P., Borregaard, N., Reithmeier, R., Lindsay, T.F., Lichtenberger, C., Reinisch, W., Lambeau, G., Arm, J., Tischfield, J., Gelb, M.H., Rubin, B.B. J. Biol. Chem. (2002) [Pubmed]
  27. The synthetic peptide Trp-Lys-Tyr-Met-Val-D-Met inhibits human monocyte-derived dendritic cell maturation via formyl peptide receptor and formyl peptide receptor-like 2. Kang, H.K., Lee, H.Y., Kim, M.K., Park, K.S., Park, Y.M., Kwak, J.Y., Bae, Y.S. J. Immunol. (2005) [Pubmed]
  28. Interleukin-8 (IL-8), melanoma growth-stimulatory activity, and neutrophil-activating peptide selectively mediate priming of the neutrophil NADPH oxidase through the type A or type B IL-8 receptor. Green, S.P., Chuntharapai, A., Curnutte, J.T. J. Biol. Chem. (1996) [Pubmed]
  29. ADP-ribosylation factor 1-regulated phospholipase D activity is localized at the plasma membrane and intracellular organelles in HL60 cells. Whatmore, J., Morgan, C.P., Cunningham, E., Collison, K.S., Willison, K.R., Cockcroft, S. Biochem. J. (1996) [Pubmed]
  30. CP-64131, an aminobenzazepine with cytokine-like properties, stimulates human neutrophil functions through the p38-MAPK pathway. Anderson, M.S., Knall, C., Thurman, G., Mann, D., Cusack, N., Johnson, G.L., Ambruso, D.R. J. Leukoc. Biol. (2004) [Pubmed]
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