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H3 phosphorylation and transcriptional regulation

Phosphorylation of H3 is not limited to mitosis and also occurs in G1 phase of the cell cycle. Activation of the Ras-Raf-MEK-ERK signal transduction pathway and/or of the p38 stress kinase pathway when cells are treated with epidermal growth factor (EGF), 12-G-tetradecanoylphorbol-13-acetate (TPA), anesomycin, okadiac acid, and stresses such as UV irradiation induces the rapid phosphorylation of H3 at Ser-10 and/or Ser-28 [68-72] (Figs. 5 and 6). Inhibition of the MEK1,2 activity with PD98059 prevents the activation of ERK and TPA-induced H3 [Pg.211]

Stimulation of ovarian granulosa cells with follicle-stimulating hormone results in the phosphorylation of H3 at Ser-10 [74]. However, neither the Ras-Raf-MEK-ERK signal transduction nor the p38 stress kinase pathways are involved in this response. [Pg.212]


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