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本文引用的文献

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Activation and regulation of ATM kinase activity in response to DNA double-strand breaks.响应DNA双链断裂时ATM激酶活性的激活与调控。
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Shaping genetic alterations in human cancer: the p53 mutation paradigm.塑造人类癌症中的基因改变：p53突变范例
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The carboxy terminus of NBS1 is required for induction of apoptosis by the MRE11 complex.NBS1的羧基末端是MRE11复合物诱导细胞凋亡所必需的。
Nature. 2007 May 10;447(7141):218-21. doi: 10.1038/nature05740. Epub 2007 Apr 11.
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The breast cancer susceptibility allele CHEK2*1100delC promotes genomic instability in a knock-in mouse model.乳腺癌易感等位基因CHEK2*1100delC在基因敲入小鼠模型中促进基因组不稳定。
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p21 delays tumor onset by preservation of chromosomal stability.p21通过维持染色体稳定性来延迟肿瘤发生。
Proc Natl Acad Sci U S A. 2006 Dec 26;103(52):19842-7. doi: 10.1073/pnas.0606343104. Epub 2006 Dec 14.
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Cellular functions of the BRCA tumour-suppressor proteins.BRCA肿瘤抑制蛋白的细胞功能。
Biochem Soc Trans. 2006 Nov;34(Pt 5):633-45. doi: 10.1042/BST0340633.
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The CHEK2 gene and inherited breast cancer susceptibility.CHEK2基因与遗传性乳腺癌易感性。
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8
Methods for studying the cellular response to DNA damage: influence of the Mre11 complex on chromosome metabolism.研究细胞对DNA损伤反应的方法：Mre11复合物对染色体代谢的影响
Methods Enzymol. 2006;409:251-84. doi: 10.1016/S0076-6879(05)09015-4.
9
Ser18 and 23 phosphorylation is required for p53-dependent apoptosis and tumor suppression.p53依赖的细胞凋亡和肿瘤抑制需要Ser18和23位点的磷酸化。
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ATR dependent activation of Chk2.ATR依赖的Chk2激活。
J Cell Physiol. 2006 Sep;208(3):613-9. doi: 10.1002/jcp.20700.

Chk2抑制与DNA复制相关的DNA损伤的致癌潜能。

Chk2 suppresses the oncogenic potential of DNA replication-associated DNA damage.

作者信息

Stracker Travis H, Couto Suzana S, Cordon-Cardo Carlos, Matos Tulio, Petrini John H J

机构信息

Molecular Biology Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, Cornell University Graduate School of Medical Sciences, New York, NY 10021, USA.

出版信息

Mol Cell. 2008 Jul 11;31(1):21-32. doi: 10.1016/j.molcel.2008.04.028.

DOI:10.1016/j.molcel.2008.04.028
PMID:18614044
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2586815/
Abstract

The Mre11 complex (Mre11, Rad50, and Nbs1) and Chk2 have been implicated in the DNA-damage response, an inducible process required for the suppression of malignancy. The Mre11 complex is predominantly required for repair and checkpoint activation in S phase, whereas Chk2 governs apoptosis. We examined the relationship between the Mre11 complex and Chk2 in the DNA-damage response via the establishment of Nbs1(DeltaB/DeltaB) Chk2(-/-) and Mre11(ATLD1/ATLD1) Chk2(-/-) mice. Chk2 deficiency did not modify the checkpoint defects or chromosomal instability of Mre11 complex mutants; however, the double-mutant mice exhibited synergistic defects in DNA-damage-induced p53 regulation and apoptosis. Nbs1(DeltaB/DeltaB) Chk2(-/-) and Mre11(ATLD1/ATLD1) Chk2(-/-) mice were also predisposed to tumors. In contrast, DNA-PKcs-deficient mice, in which G1-specific chromosome breaks are present, did not exhibit synergy with Chk2(-/-) mutants. These data suggest that Chk2 suppresses the oncogenic potential of DNA damage arising during S and G2 phases of the cell cycle.

摘要

Mre11复合物（Mre11、Rad50和Nbs1）和Chk2参与了DNA损伤反应，这是抑制恶性肿瘤所需的一个可诱导过程。Mre11复合物主要在S期的修复和检查点激活中发挥作用，而Chk2则调控细胞凋亡。我们通过构建Nbs1(DeltaB/DeltaB)Chk2(-/-)和Mre11(ATLD1/ATLD1)Chk2(-/-)小鼠，研究了DNA损伤反应中Mre11复合物与Chk2之间的关系。Chk2缺陷并未改变Mre11复合物突变体的检查点缺陷或染色体不稳定性；然而，双突变小鼠在DNA损伤诱导的p53调控和细胞凋亡方面表现出协同缺陷。Nbs1(DeltaB/DeltaB)Chk2(-/-)和Mre11(ATLD1/ATLD1)Chk2(-/-)小鼠也易患肿瘤。相比之下，存在G1期特异性染色体断裂的DNA-PKcs缺陷小鼠，并未与Chk2(-/-)突变体表现出协同作用。这些数据表明，Chk2抑制了细胞周期S期和G2期期间产生的DNA损伤的致癌潜力。