Fig. 1.

p38 MAPK inflammatory signalling is regulated by PP2A. p38 MAPK activates MK2, subsequently mediating the phosphorylation and thereby the inactivation of TTP. Inactive TTP allows for the stabilisation of pro-inflammatory cytokine mRNA and thus sustained inflammation. In response to sustained inflammation, MKP-1 acts as a negative feedback effector, dephosphorylating and thereby inactivating p38 MAPK, and inhibiting downstream pro-inflammatory signalling. PP2A dephosphorylates and activates TTP. Active TTP degrades pro-inflammatory cytokine mRNA by binding to the ARE 3′ untranslated region, resulting in the suppression of inflammation