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Cell Cycle. 2013 Jan 15;12(2):332-45. doi: 10.4161/cc.23177. Epub 2012 Jan 15.
3
Identification of the first ATRIP-deficient patient and novel mutations in ATR define a clinical spectrum for ATR-ATRIP Seckel Syndrome.鉴定首个 ATRIP 缺陷患者和 ATR 中的新突变，为 ATR-ATRIP 型 Seckel 综合征定义了临床谱。
PLoS Genet. 2012;8(11):e1002945. doi: 10.1371/journal.pgen.1002945. Epub 2012 Nov 8.
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A prognostic signature of defective p53-dependent G1 checkpoint function in melanoma cell lines.黑色素瘤细胞系中 p53 依赖性 G1 检验点功能缺陷的预后标志。
Pigment Cell Melanoma Res. 2012 Jul;25(4):514-26. doi: 10.1111/j.1755-148X.2012.01010.x. Epub 2012 Jun 1.
5
Kinase-independent function of checkpoint kinase 1 (Chk1) in the replication of damaged DNA.有丝分裂检查点激酶 1（Chk1）在损伤 DNA 复制中的激酶非依赖性功能。
Proc Natl Acad Sci U S A. 2012 May 8;109(19):7344-9. doi: 10.1073/pnas.1116345109. Epub 2012 Apr 23.
6
Germline mutation in ATR in autosomal- dominant oropharyngeal cancer syndrome.常染色体显性遗传口咽癌综合征中的 ATR 种系突变。
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7
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Dbf4 is direct downstream target of ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3-related (ATR) protein to regulate intra-S-phase checkpoint.Dbf4 是共济失调毛细血管扩张突变（ATM）和共济失调毛细血管扩张和 Rad3 相关（ATR）蛋白的直接下游靶点，以调节细胞内 S 期检查点。
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Xeroderma pigmentosum.着色性干皮病。
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Analyzing DNA replication dynamics of genotoxin-treated cells using velocity sedimentation.使用速度沉降法分析基因毒素处理细胞的DNA复制动力学。
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人成纤维细胞内 S 期检验点的激活是否是防止 UV 诱导突变的一个重要因素？

Is activation of the intra-S checkpoint in human fibroblasts an important factor in protection against UV-induced mutagenesis?

机构信息

Curriculum in Toxicology; University of North Carolina-Chapel Hill; Chapel Hill, NC USA.

出版信息

Cell Cycle. 2013 Nov 15;12(22):3555-63. doi: 10.4161/cc.26590. Epub 2013 Sep 25.

DOI:10.4161/cc.26590
PMID:24091629
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3906341/
Abstract

The ATR/CHK1-dependent intra-S checkpoint inhibits replicon initiation and replication fork progression in response to DNA damage caused by UV (UV) radiation. It has been proposed that this signaling cascade protects against UV-induced mutations by reducing the probability that damaged DNA will be replicated before it can be repaired. Normal human fibroblasts (NHF) were depleted of ATR or CHK1, or treated with the CHK1 kinase inhibitor TCS2312, and the UV-induced mutation frequency at the HPRT locus was measured. Despite clear evidence of S-phase checkpoint abrogation, neither ATR/CHK1 depletion nor CHK1 inhibition caused an increase in the UV-induced HPRT mutation frequency. These results question the premise that the UV-induced intra-S checkpoint plays a prominent role in protecting against UV-induced mutagenesis.

摘要

ATR/CHK1 依赖性的 S 期检查点抑制复制起始和复制叉进展，以响应由 UV（紫外线）辐射引起的 DNA 损伤。据推测，这种信号级联反应通过降低在受损 DNA 修复之前被复制的可能性来防止 UV 诱导的突变。正常的人成纤维细胞（NHF）被耗尽 ATR 或 CHK1，或用 CHK1 激酶抑制剂 TCS2312 处理，并测量 HPRT 基因座处的 UV 诱导突变频率。尽管有明显的 S 期检查点中断的证据，但 ATR/CHK1 耗尽或 CHK1 抑制均不会导致 UV 诱导的 HPRT 突变频率增加。这些结果质疑了 UV 诱导的 S 期检查点在防止 UV 诱导的突变中起主要作用的前提。