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从PKA到MPF途径调控卵细胞减数分裂周期的研究进展

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摘要 在大多数物种中,由于未知的体内信号作用,细胞减数分裂周期停滞在分裂前期到中期的过渡阶段。在促黄体激素作用下,Cdc2/cyclinB复合物(即MPF)的Cdc2激酶组分被活化,进而促发胚泡破裂。这种现象的内在机制为高浓度的cAMP及活化的PKA导致Cdc25B及Wee1b磷酸化从而使Cdc25B失活及Wee1b活化,活化的蛋白激酶Wee1b磷酸化Cdc2使MPF失活,从而使减数分裂停滞在分裂前期。在促黄体激素的作用下,最终导致MPF再次活化,减数分裂重新开始。
出处 《中国当代医药》 2011年第13期23-24,共2页 China Modern Medicine
关键词 MPF PKA CDC25B Wee1b
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参考文献12

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