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首页> 外文期刊>Molecular and Cellular Biology >JunB Breakdown in Mid-/Late G2 Is Required for Down-Regulation of Cyclin A2 Levels and Proper Mitosis
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JunB Breakdown in Mid-/Late G2 Is Required for Down-Regulation of Cyclin A2 Levels and Proper Mitosis

机译：下调细胞周期蛋白A2水平和适当的有丝分裂需要G2中/晚期的JunB分解

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JunB, a member of the AP-1 family of dimeric transcription factors, is best known as a cell proliferation inhibitor, a senescence inducer, and a tumor suppressor, although it also has been attributed a cell division-promoting activity. Its effects on the cell cycle have been studied mostly in G1 and S phases, whereas its role in G2 and M phases still is elusive. Using cell synchronization experiments, we show that JunB levels, which are high in S phase, drop during mid- to late G2 phase due to accelerated phosphorylation-dependent degradation by the proteasome. The forced expression of an ectopic JunB protein in late G2 phase indicates that JunB decay is necessary for the subsequent reduction of cyclin A2 levels in prometaphase, the latter event being essential for proper mitosis. Consistently, abnormal JunB expression in late G2 phase entails a variety of mitotic defects. As these aberrations may cause genetic instability, our findings contrast with the acknowledged tumor suppressor activity of JunB and reveal a mechanism by which the deregulation of JunB might contribute to tumorigenesis.
机译：JunB是二元转录因子AP-1家族的成员，尽管它也被认为具有促进细胞分裂的活性，但它作为细胞增殖抑制剂，衰老诱导剂和肿瘤抑制剂最为人所知。大部分在G 1 和S期研究了其对细胞周期的影响，而在G 2 和M期的作用尚不清楚。使用细胞同步实验，我们发现，由于蛋白酶体加速的磷酸化依赖性降解，S期中较高的JunB水平在G 2 中后期出现下降。异位JunB蛋白在G 2 晚期的强制表达表明，JunB衰变对于随后减少前中期细胞周期蛋白A2的水平是必要的，后者对于适当的有丝分裂是必不可少的。一致地，G 2 后期晚期的JunB表达异常会导致多种有丝分裂缺陷。由于这些畸变可能会导致遗传不稳定，因此我们的发现与公认的JunB抑癌活性形成对比，并揭示了JunB失控可能有助于肿瘤发生的机制。

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