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Blocking transcription of the human rhodopsin gene by triplex-mediated DNA photocrosslinking.通过三链介导的DNA光交联阻断人视紫红质基因的转录。
Nucleic Acids Res. 2000 Nov 1;28(21):4283-90. doi: 10.1093/nar/28.21.4283.
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Psoralen photo-cross-linking by triplex-forming oligonucleotides at multiple sites in the human rhodopsin gene.由三链形成寡核苷酸在人视紫红质基因多个位点进行的补骨脂素光交联。
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Asymmetric recognition of psoralen interstrand crosslinks by the nucleotide excision repair and the error-prone repair pathways.核苷酸切除修复和易错修复途径对补骨脂素链间交联的不对称识别。
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本文引用的文献

1
Psoralen adducts induced by triplex-forming oligonucleotides are refractory to repair in HeLa cells.由三链形成寡核苷酸诱导的补骨脂素加合物在HeLa细胞中难以修复。
J Mol Biol. 2000 Feb 18;296(2):373-83. doi: 10.1006/jmbi.1999.3466.
2
Triple helix-forming oligonucleotides target psoralen adducts to specific chromosomal sequences in human cells.形成三链螺旋的寡核苷酸将补骨脂素加合物靶向人类细胞中的特定染色体序列。
Nucleic Acids Res. 1999 Dec 15;27(24):4734-42. doi: 10.1093/nar/27.24.4734.
3
Psoralen photo-cross-linking by triplex-forming oligonucleotides at multiple sites in the human rhodopsin gene.由三链形成寡核苷酸在人视紫红质基因多个位点进行的补骨脂素光交联。
Biochemistry. 1999 Sep 28;38(39):12850-9. doi: 10.1021/bi9902743.
4
Chromosomal mutations induced by triplex-forming oligonucleotides in mammalian cells.三链形成寡核苷酸在哺乳动物细胞中诱导的染色体突变。
Nucleic Acids Res. 1999 Feb 15;27(4):1176-81. doi: 10.1093/nar/27.4.1176.
5
Morphological, physiological, and biochemical changes in rhodopsin knockout mice.视紫红质基因敲除小鼠的形态学、生理学和生化变化。
Proc Natl Acad Sci U S A. 1999 Jan 19;96(2):736-41. doi: 10.1073/pnas.96.2.736.
6
A novel mutation within the rhodopsin gene (Thr-94-Ile) causing autosomal dominant congenital stationary night blindness.视紫红质基因内一个新的突变(苏氨酸-94-异亮氨酸)导致常染色体显性遗传性先天性静止性夜盲。
Hum Mutat. 1999;13(1):75-81. doi: 10.1002/(SICI)1098-1004(1999)13:1<75::AID-HUMU9>3.0.CO;2-4.
7
Targeted gene knockout mediated by triple helix forming oligonucleotides.由三链螺旋形成寡核苷酸介导的靶向基因敲除。
Nat Genet. 1998 Oct;20(2):212-4. doi: 10.1038/2530.
8
Triplex targets in the human rhodopsin gene.人类视紫红质基因中的三链体靶点。
Biochemistry. 1998 Aug 11;37(32):11315-22. doi: 10.1021/bi980525s.
9
Synthetic activation of caspases: artificial death switches.半胱天冬酶的合成激活:人工死亡开关
Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):3655-60. doi: 10.1073/pnas.95.7.3655.
10
Triplex-directed modification of genes and gene activity.基因和基因活性的三链引导修饰。
Trends Biochem Sci. 1998 Jan;23(1):4-9. doi: 10.1016/s0968-0004(97)01158-4.

通过三链介导的DNA光交联阻断人视紫红质基因的转录。

Blocking transcription of the human rhodopsin gene by triplex-mediated DNA photocrosslinking.

作者信息

Intody Z, Perkins B D, Wilson J H, Wensel T G

机构信息

Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.

出版信息

Nucleic Acids Res. 2000 Nov 1;28(21):4283-90. doi: 10.1093/nar/28.21.4283.

DOI:10.1093/nar/28.21.4283
PMID:11058128
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC113126/
Abstract

To explore the ability of triplex-forming oligodeoxyribonucleotides (TFOs) to inhibit genes responsible for dominant genetic disorders, we used two TFOs to block expression of the human rhodopsin gene, which encodes a G protein-coupled receptor involved in the blinding disorder autosomal dominant retinitis pigmentosa. Psoralen-modified TFOs and UVA irradiation were used to form photoadducts at two target sites in a plasmid expressing a rhodopsin-EGFP fusion, which was then transfected into HT1080 cells. Each TFO reduced rhodopsin-GFP expression by 70-80%, whereas treatment with both reduced expression by 90%. Expression levels of control genes on either the same plasmid or one co-transfected were not affected by the treatment. Mutations at one TFO target eliminated its effect on transcription, without diminishing inhibition by the other TFO. Northern blots indicated that TFO-directed psoralen photoadducts blocked progression of RNA polymerase, resulting in truncated transcripts. Inhibition of gene expression was not relieved over a 72 h period, suggesting that TFO-induced psoralen lesions are not repaired on this time scale. Irradiation of cells after transfection with plasmid and psoralen-TFOs produced photoadducts inside the cells and also inhibited expression of rhodopsin-EGFP. We conclude that directing DNA damage with psoralen-TFOs is an efficient and specific means for blocking transcription from the human rhodopsin gene.

摘要

为了探索三链形成寡脱氧核糖核苷酸(TFOs)抑制导致显性遗传病的基因的能力,我们使用了两种TFOs来阻断人类视紫红质基因的表达,该基因编码一种参与致盲疾病常染色体显性视网膜色素变性的G蛋白偶联受体。补骨脂素修饰的TFOs和紫外线A照射用于在表达视紫红质-增强绿色荧光蛋白(rhodopsin-EGFP)融合蛋白的质粒中的两个靶位点形成光加合物,然后将其转染到HT1080细胞中。每种TFO将视紫红质-绿色荧光蛋白的表达降低了70%-80%,而两种TFO共同处理则将表达降低了90%。同一质粒上或共转染的一个对照基因的表达水平不受该处理的影响。一个TFO靶位点的突变消除了其对转录的影响,但并未削弱另一个TFO的抑制作用。Northern印迹表明,TFO引导的补骨脂素光加合物阻断了RNA聚合酶的进程,导致转录本截短。在72小时内基因表达的抑制并未解除,这表明在这个时间尺度上TFO诱导的补骨脂素损伤未得到修复。用质粒和补骨脂素-TFOs转染细胞后进行照射,在细胞内产生了光加合物,同时也抑制了视紫红质-EGFP的表达。我们得出结论,用补骨脂素-TFOs引导DNA损伤是阻断人类视紫红质基因转录的一种有效且特异的方法。