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. - In: FEBS LETTERS. - ISSN 0014-5793. - 587:10(2013), pp. 1536-1542. [10.1016/j.febslet.2013.03.036.]
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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
