Journal
FEBS LETTERS
Volume 587, Issue 10, Pages 1536-1542Publisher
WILEY
DOI: 10.1016/j.febslet.2013.03.036
Keywords
FPR2; c-Met; NADPH oxidase; Transactivation; Signal transduction
Funding
- Ministero dell'Istruzione, dell'Universita e della Ricerca PRIN
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Cross-communication between GPCRs and TKRs represents a mechanism to amplify the information exchange throughout the cell. We show that WKYMVm, an FPR2 agonist, induces the phosphorylation of Y1313/Y1349/Y1356 residues of c-Met and triggers some of the molecular responses elicited by c-Met/HGF binding, such as STAT3, PLC-gamma 1/PKC alpha and PI3K/Akt pathways. The critical role of NADPH oxidase-dependent superoxide generation in this cross-talk mechanism is supported by the finding that blockade of NADPH oxidase function prevents c-Met trans-phosphorylation and the downstream signalling cascade. These results highlight the function of FPR2 to activate a interconnected signalling network and suggest novel possibilities for therapeutic interventions. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
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