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Nucleotide Excision Repair01:08

Nucleotide Excision Repair

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Base Excision Repair01:54

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One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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Long-patch Base Excision Repair01:02

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Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
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Translesion DNA Polymerases02:10

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Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
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Conservative Site-specific Recombination and Phase Variation02:53

Conservative Site-specific Recombination and Phase Variation

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Because the DNA segments are cut and reorganized in a direction-specific manner, site-specific recombination has emerged as an efficient genetic engineering technique. Flippase and Cyclization recombinases or Flp and Cre, respectively, are two members of the tyrosine recombinase family derived from bacteriophages, that are used to mediate site-specific DNA insertions, deletions, and targeted expression of proteins in mammalian cell lines.
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这页已由机器翻译。其他页面可能仍然显示为英文。View in English
  1. 首页
  2. 研究领域
  3. 工程学
  4. 纳米技术
  5. 纳米学
  6. 由于rna编辑影响的neil1重编 损伤特异性识别和切除

由于RNA编辑影响的NEIL1重编 损伤特异性识别和切除

Elizabeth R Lotsof1, Allison E Krajewski2, Brittany Anderson-Steele1

  • 1Department of Chemistry, University of California, Davis, Davis, California 95616, United States.

Journal of the American Chemical Society
|August 2, 2022

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Atomic Force Microscopy Investigations of DNA Lesion Recognition in Nucleotide Excision Repair
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Atomic Force Microscopy Investigations of DNA Lesion Recognition in Nucleotide Excision Repair

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Proofreading and DNA Repair Assay Using Single Nucleotide Extension and MALDI-TOF Mass Spectrometry Analysis
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Proofreading and DNA Repair Assay Using Single Nucleotide Extension and MALDI-TOF Mass Spectrometry Analysis

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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

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在PubMed 上查看摘要

概括
此摘要是机器生成的。

A-to-I RNA编辑修改了NEIL1的DNA修复酶,从而产生了不同的异型. 这些异构体在去除不同氧化DNA损伤方面表现出不同的效率,影响DNA修复途径.

科学领域:

  • 分子生物学
  • 生物化学
  • 遗传学

背景情况:

  • A-to-I RNA编辑在人类中很常见,但在神经系统以外的编码区域很少见.
  • 基切除DNA修复酶NEIL1异常地被ADAR1重新编码.
  • 这种编辑在NEIL1的病变识别循环中将素转化为氨酸,改变其基质特异性.

研究的目的:

  • 研究A-to-IRNA编辑如何影响NEIL1的DNA修复活动.
  • 了解影响氧化损坏的DNA基的异形特异性修复的化学和结构特征.

主要方法:

  • 酶活性测定比较未经编辑的 (UE) 和编辑的 (Ed) NEIL1异型.
  • 对各种氧化修饰DNA基的修复效率的评估.
  • 气相计算以分析基损伤特性.

主要成果:

  • UE NEIL1对氧化皮里米丁 (例如胺糖醇,乌拉糖醇) 的活性较高.
  • 而NEIL1在去除5-基细胞素和瓜尼迪诺胺方面更有效.
  • 切割速率与基稳定性和质子亲和力相关.

结论:

  • NEIL1编辑创建具有独特基质特性的功能性异构体.

相关实验视频

Atomic Force Microscopy Investigations of DNA Lesion Recognition in Nucleotide Excision Repair
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Atomic Force Microscopy Investigations of DNA Lesion Recognition in Nucleotide Excision Repair

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Proofreading and DNA Repair Assay Using Single Nucleotide Extension and MALDI-TOF Mass Spectrometry Analysis
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Proofreading and DNA Repair Assay Using Single Nucleotide Extension and MALDI-TOF Mass Spectrometry Analysis

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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

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  • 化和N3质子化是NEIL1对胺损伤的催化机制的关键.
  • 复杂的NEIL1活动表明它在DNA修复和表观遗传调节中的作用.