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-??1/PKC?? 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.

WKYMVm-induced cross-talk between FPR2 and HGF receptor in human prostate epithelial cell line PNT1A.

CATTANEO, FABIO;PARISI, MELANIA;AMMENDOLA, ROSARIO
2013

Abstract

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-??1/PKC?? 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.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/565971
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