Functional similarities and uniqueness of p27 and p57: Insight from a knock-in mouse model
Functional similarities and uniqueness of p27 and p57: Insight from a knock-in mouse model
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DOI：
10.4161/cc.8.16.9330
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发表时间：
2009-08
期刊：
影响因子：
4.3
通讯作者：
E. Susaki;K. Nakayama
中科院分区：
文献类型：
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作者：
E. Susaki;K. Nakayama
细胞周期蛋白依赖性激酶抑制剂（CKIs）p27和p57在结构上相似，并且它们的生物化学和细胞功能被认为是等同的。然而，缺乏p27或p57的小鼠表现出明显不同的表型，这表明这两种蛋白质在体内的作用可能不同。为了解决这一明显的差异，我们已经产生了一个敲入小鼠模型，其中内源性p57基因被p27基因取代，从而表达p27而不是p57。该小鼠模型提供了证据，证明p57在体内作为真正的CKI发挥作用，并且其大部分作用可以由p27执行。我们的研究结果还强调并提供了深入了解的问题，是什么决定了不同的细胞反应异常细胞周期诱导的CKIs的损失。
The cyclin-dependent kinase inhibitors (CKIs) p27 and p57 are structurally similar, and their biochemical and cellular functions have been thought to be equivalent. However, mice deficient in either p27 or p57 exhibit markedly different phenotypes, suggesting that the in vivo roles of these two proteins might differ. To address this apparent discrepancy, we have generated a knock-in mouse model in which the endogenous p57 gene is replaced by the p27 gene, with p27 thus being expressed instead of p57. This mouse model has provided evidence that p57 functions as a bona fide CKI in vivo and that most of its roles can be performed by p27. Our findings also highlight and provide insight into the question of what determines the distinct cellular responses to abnormal cell cycling induced by the loss of CKIs.