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      MAPK3/1 (ERK1/2) in ovarian granulosa cells are essential for female fertility.

      Science (New York, N.Y.)
      Animals, CCAAT-Enhancer-Binding Protein-beta, genetics, metabolism, Enzyme Activation, Female, Fertility, Gene Expression Profiling, Granulosa Cells, enzymology, Luteinizing Hormone, MAP Kinase Signaling System, Meiosis, Mice, Mice, Inbred C57BL, Mice, Transgenic, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Oocytes, physiology, Ovarian Follicle, Ovulation, Phosphorylation

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          A surge of luteinizing hormone (LH) from the pituitary gland triggers ovulation, oocyte maturation, and luteinization for successful reproduction in mammals. Because the signaling molecules RAS and ERK1/2 (extracellular signal-regulated kinases 1 and 2) are activated by an LH surge in granulosa cells of preovulatory follicles, we disrupted Erk1/2 in mouse granulosa cells and provide in vivo evidence that these kinases are necessary for LH-induced oocyte resumption of meiosis, ovulation, and luteinization. In addition, biochemical analyses and selected disruption of the Cebpb gene in granulosa cells demonstrate that C/EBPbeta (CCAAT/Enhancer-binding protein-beta) is a critical downstream mediator of ERK1/2 activation. Thus, ERK1/2 and C/EBPbeta constitute an in vivo LH-regulated signaling pathway that controls ovulation- and luteinization-related events.

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