抑癌作用中的休眠起始点。
A role for dormant origins in tumor suppression.
机构信息
Wellcome Trust Centre for Gene Regulation and Expression, University of Dundee, Dow Street, Dundee DD1 5EH, UK.
出版信息
Mol Cell. 2011 Mar 4;41(5):495-6. doi: 10.1016/j.molcel.2011.02.014.
Abstract
In this issue of Molecular Cell, Kawabata et al. (2011) show that mice hypomorphic for the replication licensing protein Mcm4 show spontaneous DNA replication defects due to a lack of dormant origins, potentially explaining why these mice are cancer-prone.
摘要
在本期《分子细胞》中，Kawabata 等人（2011 年）表明，由于缺乏休眠起始点，Mcm4 复制许可蛋白功能减弱的小鼠表现出自发的 DNA 复制缺陷，这可能解释了为什么这些小鼠容易患癌症。
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本文引用的文献
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Mol Cell. 2011 Mar 4;41(5):543-53. doi: 10.1016/j.molcel.2011.02.006.
2
DNA damage response and tumorigenesis in Mcm2-deficient mice.Mcm2 缺陷小鼠的 DNA 损伤反应与肿瘤发生。
Oncogene. 2010 Jun 24;29(25):3630-8. doi: 10.1038/onc.2010.125. Epub 2010 May 3.
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EMBO Rep. 2009 Apr;10(4):406-12. doi: 10.1038/embor.2009.5. Epub 2009 Feb 13.
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Nat Rev Cancer. 2008 Oct;8(10):799-806. doi: 10.1038/nrc2500. Epub 2008 Aug 29.
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