有丝分裂期间的Chk1磷酸化：一种主要调节因子的新作用。
Chk1 phosphorylation during mitosis: a new role for a master regulator.
作者信息
Wilsker Deborah, Bunz Fred
机构信息
Department of Radiation Oncology and Molecular Radiation Sciences, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
出版信息
Cell Cycle. 2009 Apr 15;8(8):1161-3. doi: 10.4161/cc.8.8.8148. Epub 2009 Apr 11.
Abstract
The human DNA damage responses are modulated by both nonessential and essential pathways. The extensively studied ATM kinase and p53 are examples of the former. While loss-of-function mutations in genes that encode ATM and p53 cause marked predispositions to cancer, the loss of these proteins does not appear to impact basic cell growth and proliferation. In contrast, the checkpoint kinase Chk1 and its upstream activator ATR are essential.(1-4) What do these proteins do in undamaged cells?
摘要
人类的DNA损伤反应由非必需途径和必需途径共同调节。被广泛研究的ATM激酶和p53就是前者的例子。虽然编码ATM和p53的基因功能丧失突变会显著增加患癌倾向，但这些蛋白质的缺失似乎并不影响细胞的基本生长和增殖。相比之下，检查点激酶Chk1及其上游激活剂ATR是必需的。（1-4）这些蛋白质在未受损细胞中起什么作用？
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