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University of Minnesota, Hormel Institute, Austin, MN 55912
SUMMARY
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?
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