国家重点基础研究发展规划项目(973)(G1999055902)和中国科学院知识创新工程重要方向资助项目(KSCX2-SW-303).
This work was supported by grants from the Special Funds for Major State Basic Research of China (G1999055902) and Knowledge Innovation Project of The Chinese Academy of Sciences(KSCX2-SW-303).
丝裂原活化蛋白激酶(MAPK)信号途径对减数分裂有重要调节作用,p90rsk是迄今研究最清楚的MAPK下游靶分子,介导MAPK途径在卵母细胞减数分裂中的多种功能,包括卵母细胞减数分裂的启动、MⅠ/MⅡ期转化和MⅡ期阻滞的维持等.p90rsk的磷酸化是MAPK激活的结果,而细胞退出减数分裂时,p90rsk的去磷酸化也发生在MAPK失活以后.介绍了在卵母细胞中p90rsk的研究进展.
Mitogen-activated protein kinase (MAPK) signaling pathway plays important roles in the meiosis of oocytes. p90rsk is the best known target of MAPK, which mediates multiple functions of MAPK during oocyte meiotic maturation, including the resumption of meiosis, the MⅠ/MⅡ transition and the sustain of MⅡ arrest. The phosphorylation of p90rsk is the result of MAPK activation, and the dephosphorylation of p90rsk is following the inactivation of MAPK at the end of meiosis. The progress of p90rsk in oocytes is introduced.
范衡宇,佟超,孙青原.核糖体S6蛋白激酶p90rsk与卵母细胞减数分裂[J].生物化学与生物物理进展,2002,29(4):506-509
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