Fig. 11. Working model for the regulation of p44ERK activity in RTHD fibroblasts during chemical anoxia/recovery. Our data suggest that p38^MAPK inhibits ERK activity at the level of MEK during chemical anoxia. During recovery, we demonstrated the requirement for ROS, produced via a NAD(P)H oxidase-like activity for reactivation of ERK in a Raf-independent manner. We speculate that ROS results in activation of Src, which in turn activates PKC upstream of MEKK1.