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Characterization of p70 S6 kinase 1 in early development of mouse embryos.

机译:p70 S6激酶1在小鼠胚胎早期发育中的特征。

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摘要

The mTOR kinase controls cell growth, proliferation, and survival through two distinct multiprotein complexes mTORC1 and mTORC2. p70 S6 Kinase 1 (S6K1) is characterized as downstream effector of mTOR. Until recently, the connection between S6K1 and mTORC1 /mTORC2 during the early development of mouse embryos has not been well elucidated. Here, the expression level of total S6K1 and its phosphorylation at Thr389 was determined in four phases of one-cell embryos. S6K1 was active throughout the cell cycle especially with higher activity in G2 and M phases. Rapamycin decreased the activity of M-phase promoting factor (MPF) and delayed the first mitotic cleavage. Down-regulating mTOR and raptor reduced S6K1 phosphorylation at Thr389 in one-cell embryos. Furthermore, rapamycin and microinjection of raptor shRNA decreased the immunofluorescent staining of Thr389 phospho-S6K1. It is proposed that mTORC1 may be involved in the control of MPF by regulating S6K1 during the early development of mouse embryos.
机译:mTOR激酶通过两种不同的多蛋白复合物mTORC1和mTORC2控制细胞的生长,增殖和存活。 p70 S6激酶1(S6K1)被表征为mTOR的下游效应子。直到最近,还没有很好地阐明小鼠胚胎早期发育过程中S6K1和mTORC1 / mTORC2之间的联系。在这里,在单细胞胚胎的四个阶段确定总S6K1的表达水平及其在Thr389的磷酸化。 S6K1在整个细胞周期中均具有活性,特别是在G2和M期具有较高的活性。雷帕霉素降低了M期促进因子(MPF)的活性,并延迟了第一次有丝分裂的裂解。下调mTOR和猛禽减少了单细胞胚胎在Thr389处的S6K1磷酸化。此外,雷帕霉素和猛禽shRNA的显微注射降低了Thr389磷酸化S6K1的免疫荧光染色。建议在小鼠胚胎的早期发育过程中,通过调节S6K1,mTORC1可能参与MPF的控制。

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