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Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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TRAIP是DNA跨链修复的一个主调节器

R Alex Wu1, Daniel R Semlow1, Ashley N Kamimae-Lanning2

  • 1Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, USA.

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|March 8, 2019
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概括

TRAIP控制了DNA修复途径的选择. 它通过CMG基酶无处不在激活NEIL3糖酶或触发Fanconi贫血路径修复,确保基因组的稳定性.

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科学领域:

  • 分子生物学
  • DNA 修复机制
  • 细胞对DNA损伤的反应

背景情况:

  • 通过阻断复制和转录,DNA链间交叉链 (ICL) 对基因组完整性构成重大威胁.
  • 细胞使用不同的途径来修复ICL,而途径的选择会影响修复的可靠性和基因组不稳定性的可能性.
  • 对于ICL修复途径,特别是NEIL3糖酶与Fanconi贫血途径的优先级仍然不清楚.

研究的目的:

  • 阐明不同DNA跨链修复途径之间的调节机制.
  • 确定E3无素连接酶TRAIP在复制合ICL修复中的作用.
  • 了解TRAIP如何影响修复因子的招募和停滞不前的复制分叉的解决.

主要方法:

  • 使用Xenopus蛋提取物研究与ICL的复制叉碰撞.
  • 研究了TRAIP在CMG复制酶上的无处不在活性.
  • 在不同的修复结果中分析了NEIL3的差异性招募和p97 ATPase的需求.

主要成果:

  • 在NEIL3和Fanconi贫血修复途径中,TRAIP是必不可少的.
  • TRAIP使CMG酶无处不在,短的无处不在链招募NEIL3,而较长的链则通过p97促进CMG卸载.
  • 这种TRAIP的差异性无处不在决定了细胞在ICL的直接分裂或同类重组修复之间做出选择.

结论:

  • TRAIP作为一个主调节器,控制ICL修复路径之间的切换.
  • 对于解决与复制相关的DNA损伤,TRAIP对CMG无处不在和卸载的调节至关重要.
  • 这些发现为DNA复制压力期间保持基因组稳定提供了关键的见解.