Several distinct mitogen-activated protein kinase (MAPK) pathways have been identified, including the extracellular signal-regulated
kinase 1 and 2 (ERK 1-2), p38, ERK5, and c-Jun N-terminal kinase (JNK) cascades. Given that crosstalk exists between intracellular
signaling “pathways,” it seems obvious that some level of regulation must exist to prevent competing (or parallel) signals
from sending conflicting (or amplified) signals to downstream effectors. New evidence suggests that the JNK pathway inhibits
signaling by the ERK pathway by uncoupling ERK from its upstream activator MEK (MAPK/ERK kinase), thereby promoting JNK-mediated
signals to the transcriptional activator c-Jun. Does the JNK pathway function to inhibit ERK signals in general, or is this
a cell type-specific phenomenon?