Fig. 9.

Scheme summarizing proposed interactions between NGF signaling and apoptotic pathways. NGF induces at least three signals: the sustained activation of MAPK/ERK and Akt, and suppression of JNK and c-Jun phosphorylation. In the absence of NGF, JNK is activated, whereas ERK1/2 and Akt are inactivated. In the presence of NGF, araC treatment causes elevation of p53 and apoptosis without affecting NGF signaling. ERK1/2, however, suppresses signaling downstream of p53, thereby delaying apoptosis. Inhibition of the ERK pathway with PD98059 primarily eliminates this suppression, suggesting that the lack of ERK activity caused by NGF withdrawal may therefore account for the acceleration in the rate of apoptosis induced by araC.