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Schematic representation of a model indicating the role of p38 in oncogenic ras-induced premature senescence in primary fibroblasts. Activation of the Raf-MEK-ERK pathway by oncogenic ras confers cell proliferation through transcription factor AP-1, as suggested in previously published literature, and concurrently leads to premature senescence by stimulating the activity of the p38 pathway, whose activation is sufficient to induce the accumulation of p53 and p16INK4A.
