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本文引用的文献

1
Cell cycle arrest and apoptosis provoked by UV radiation-induced DNA damage are transcriptionally highly divergent responses.紫外线辐射诱导的DNA损伤所引发的细胞周期停滞和凋亡是转录水平上高度不同的反应。
Nucleic Acids Res. 2003 Aug 15;31(16):4779-90. doi: 10.1093/nar/gkg675.
2
Genome-wide comparison of human keratinocyte and squamous cell carcinoma responses to UVB irradiation: implications for skin and epithelial cancer.人类角质形成细胞与鳞状细胞癌对紫外线B照射反应的全基因组比较:对皮肤癌和上皮癌的意义。
Oncogene. 2003 May 15;22(19):2993-3006. doi: 10.1038/sj.onc.1206537.
3
PUMA mediates the apoptotic response to p53 in colorectal cancer cells.PUMA介导大肠癌细胞对p53的凋亡反应。
Proc Natl Acad Sci U S A. 2003 Feb 18;100(4):1931-6. doi: 10.1073/pnas.2627984100. Epub 2003 Feb 6.
4
Ultraviolet light-induced apoptosis is associated with S-phase in primary human fibroblasts.紫外线诱导的细胞凋亡与原代人成纤维细胞的S期有关。
DNA Repair (Amst). 2002 Oct 1;1(10):811-20. doi: 10.1016/s1568-7864(02)00109-x.
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NetAffx: Affymetrix probesets and annotations.NetAffx:Affymetrix基因芯片探针集及注释
Nucleic Acids Res. 2003 Jan 1;31(1):82-6. doi: 10.1093/nar/gkg121.
6
Two UVC-induced stress response pathways in HeLa cells identified by cDNA microarray.通过cDNA微阵列鉴定出的HeLa细胞中的两条紫外线C诱导的应激反应途径。
Environ Mol Mutagen. 2002;40(2):122-8. doi: 10.1002/em.10097.
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Live or let die: the cell's response to p53.生存还是死亡:细胞对p53的反应。
Nat Rev Cancer. 2002 Aug;2(8):594-604. doi: 10.1038/nrc864.
8
Activation of caspase-9 is required for UV-induced apoptosis of human keratinocytes.
J Biol Chem. 2002 May 31;277(22):19346-52. doi: 10.1074/jbc.M200401200. Epub 2002 Mar 27.
9
Chromatin immunoprecipitation analysis fails to support the latency model for regulation of p53 DNA binding activity in vivo.染色质免疫沉淀分析无法支持体内p53 DNA结合活性调控的潜伏模型。
Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):95-100. doi: 10.1073/pnas.012283399. Epub 2001 Dec 26.
10
Effects of XPD mutations on ultraviolet-induced apoptosis in relation to skin cancer-proneness in repair-deficient syndromes.XPD突变对紫外线诱导的细胞凋亡的影响与修复缺陷综合征中皮肤癌易感性的关系。
J Invest Dermatol. 2001 Nov;117(5):1162-70. doi: 10.1046/j.0022-202x.2001.01533.x.

基因大小对紫外线诱导基因表达的调控。

Regulation of ultraviolet light-induced gene expression by gene size.

作者信息

McKay Bruce C, Stubbert Lawton J, Fowler Casey C, Smith Jennifer M, Cardamore Robin A, Spronck Jennifer C

机构信息

Centre for Cancer Therapeutics, Ottawa Regional Cancer Centre, Department of Radiology, University of Ottawa, 503 Smyth Road, Ottawa, ON, Canada K1C 5T5.

出版信息

Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6582-6. doi: 10.1073/pnas.0308181101. Epub 2004 Apr 15.

DOI:10.1073/pnas.0308181101
PMID:15087501
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC404088/
Abstract

UV light induces the expression of a wide variety of genes. At present, it is unclear how cells sense the extent of DNA damage and alter the expression of UV-induced genes appropriately. UV light induces DNA damage that blocks transcription, and the probability that a gene sustains transcription-blocking DNA damage is proportional to locus size and dose of UV light. Using colon carcinoma cells that express a temperature-sensitive variant of p53 and undergo p53-dependent apoptosis after UV irradiation, we found that the number of p53-induced genes identified by oligonucleotide microarray analysis decreased in a UV dose-dependent manner. This was associated with a statistically significant shift in the spectrum of p53-induced genes toward compact genes with fewer and smaller introns. Genes encoding proapoptotic proteins involved in the initiation of the mitochondrial apoptotic cascade were prominent among the compact p53 target genes, whereas genes encoding negative regulators of p53 and the mitochondrial apoptotic pathway were significantly larger. We propose that the shift in spectrum of UV-responsive gene expression caused by passive effects of UV lesions on transcription acts as a molecular dosimeter, ensuring the elimination of cells sustaining irreparable transcription-blocking DNA damage.

摘要

紫外线可诱导多种基因的表达。目前,尚不清楚细胞如何感知DNA损伤的程度并相应地改变紫外线诱导基因的表达。紫外线会诱导DNA损伤从而阻断转录,而一个基因遭受转录阻断性DNA损伤的概率与基因座大小和紫外线剂量成正比。利用表达p53温度敏感变体且在紫外线照射后会经历p53依赖性凋亡的结肠癌细胞,我们发现通过寡核苷酸微阵列分析鉴定出的p53诱导基因的数量呈紫外线剂量依赖性减少。这与p53诱导基因谱向内含子数量更少、更小的紧密基因发生统计学上的显著转变有关。在紧密的p53靶基因中,编码参与线粒体凋亡级联反应起始的促凋亡蛋白的基因较为突出,而编码p53和线粒体凋亡途径负调控因子的基因则明显更大。我们认为,紫外线损伤对转录的被动影响所导致的紫外线反应性基因表达谱的转变充当了一种分子剂量计,确保清除遭受无法修复的转录阻断性DNA损伤的细胞。