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Modulation of MEK/ERK activity by mortalin and PP1α in BRAF- or KRAS-mutated cancer cells. (A) Mutations in BRAF or KRAS can induce high-magnitude MEK/ERK activity. (B) Upregulated mortalin and PP1α may have a role in modulating MEK/ERK activity in certain BRAF/KRAS tumor cells because mortalin can facilitate PP1α-mediated MEK1/2 dephosphorylation. This mechanism may be important for determining the physiological outputs of MEK/ERK activity, i.e., proliferation versus growth arrest.
