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. 2009 May 8;5(5):e1000425. doi: 10.1371/journal.ppat.1000425

Figure 6. A model of P-mediated interference with PKC-dependent signaling and neuronal plasticity.

Figure 6

Diverse potentiation stimuli will trigger activation of many kinases, including PKC. In cells infected with rBDV-WT (left), this will lead to enhanced phosphorylation of P, optimal viral spread and concomitant decreased activation of endogenous PKC substrates (among which MARCKS and SNAP-25), ultimately leading to impairment on neuronal plasticity. In neurons infected with rBDV-AASS (right), mutated P does not interfere with PKC-dependent signaling and neuronal plasticity is restored. However, lack of phosphorylation of P leads to viral attenuation.