Parri Matteo, Buricchi Francesca, Taddei Maria Letizia, Giannoni Elisa, Raugei Giovanni, Ramponi Giampietro, Chiarugi Paola
Department of Biochemical Sciences, University of Florence, Via le Morgagni 50, Florence 50134, Italy.
J Biol Chem. 2005 Oct 7;280(40):34008-18. doi: 10.1074/jbc.M502879200. Epub 2005 Jul 28.
Ephrin kinases and their ephrin ligands transduce repulsion of cells in axon guidance, migration, invasiveness, and tumor growth, exerting a negative signaling on cell proliferation and adhesion. A key role of their kinase activity has been confirmed by mutant kinase inactive receptors that shift the cellular response from repulsion to adhesion. Our present study aimed to investigate the role of low molecular weight protein-tyrosine phosphatase (LMW-PTP) in ephrinA1/EphA2 signaling. LMW-PTP, by means of dephosphorylation of EphA2 kinase, negatively regulates the ephrinA1-mediated repulsive response, cell proliferation, cell adhesion and spreading, and the formation of retraction fibers, thereby confirming the relevance of the net level of tyrosine phosphorylation of Eph receptors. LMW-PTP interferes with ephrin-mediated mitogen-activated protein kinase signaling likely through inhibition of p120RasGAP binding to the activated EphA2 kinase, thereby confirming the key role of mitogen-activated protein kinase inhibition by ephrinA1 repulsive signaling. We conclude that LMW-PTP acts as a terminator of EphA2 signaling causing an efficient negative feedback loop on the biological response mediated by ephrinA1 and pointing on tyrosine phosphorylation as the main event orchestrating the repulsive response.
Ephrin激酶及其Ephrin配体在轴突导向、迁移、侵袭和肿瘤生长过程中传导细胞排斥作用,对细胞增殖和黏附发挥负向信号作用。突变的无激酶活性受体将细胞反应从排斥转变为黏附,从而证实了其激酶活性的关键作用。我们目前的研究旨在探讨低分子量蛋白酪氨酸磷酸酶(LMW-PTP)在ephrinA1/EphA2信号传导中的作用。LMW-PTP通过使EphA2激酶去磷酸化,负向调节ephrinA1介导的排斥反应、细胞增殖、细胞黏附和铺展以及收缩纤维的形成,从而证实了Eph受体酪氨酸磷酸化净水平的相关性。LMW-PTP可能通过抑制p120RasGAP与活化的EphA2激酶结合来干扰ephrin介导的丝裂原活化蛋白激酶信号传导,从而证实了ephrinA1排斥信号对丝裂原活化蛋白激酶抑制的关键作用。我们得出结论,LMW-PTP作为EphA2信号的终止子,对ephrinA1介导的生物学反应产生有效的负反馈环,并指出酪氨酸磷酸化是协调排斥反应的主要事件。