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相关概念视频

Mismatch Repair01:20

Mismatch Repair

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
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Translesion DNA Polymerases02:10

Translesion DNA Polymerases

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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.
TLS polymerases are found in all three domains of life - archaea, bacteria, and eukaryotes. Of the different classes of TLS polymerases, members of the Y family are fitted with specialized structures that...
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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.
The recognition sites for Cre recombinase called LoxP...
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Mutations01:39

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Overview
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Abnormal Proliferation02:23

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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tRNA Activation02:26

tRNA Activation

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Aminoacyl-tRNA synthetases are present in both eukaryotes and bacteria. Though eukaryotes have 20 different aminoacyl-tRNA synthetases to couple to 20 amino acids, many bacteria do not have genes for all of these aminoacyl-tRNA synthetases. Despite this, they still use all 20 amino acids to synthesize their proteins. For instance, some bacteria do not have the gene encoding the enzyme that couples glutamine with its partner tRNA. In these organisms, one enzyme adds glutamic acid to all of the...
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相关实验视频

Updated: Jun 28, 2025

Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes
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在体质超突变中服AID突变因子活性.

Yining Qin1, Fei-Long Meng1

  • 1Key Laboratory of RNA Science and Engineering, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences; Shanghai 200031, China.

Trends in biochemical sciences
|April 13, 2024
PubMed
概括

激活诱导的cytidine deaminase (AID) 可以安全地修改DNA进行抗体成熟. 了解它的规则,为纠正遗传疾病提供了基础编辑设计的信息.

关键词:
援助 援助 援助 援助这是APOBECAPOBECAPOBECAPOBECAPOBECAPOBECAPOBECAPOBECAPOBECAPOBECAPOBECAPOBECAPOBECDNA 机械学 DNA 机械学基础编辑器 基础编辑器淋巴瘤是一种淋巴瘤.

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Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches
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科学领域:

  • 免疫学 免疫学 免疫学
  • 分子生物学分子生物学
  • 遗传学 遗传学 是一个

背景情况:

  • 激活诱导的cytidine deaminase (AID) 对于通过体质突变 (SHM) 实现抗体基因多样化至关重要.
  • 艾滋病活性失调与淋巴发育有关,强调需要了解其精确的控制机制.
  • 对于AID的DNA修饰活动的精确调节仍然不完全理解.

研究的目的:

  • 阐明AID活动的多方面的监管.
  • 探索新兴的概念和影响AID精确DNA损伤发生的因素.
  • 讨论AID监管对开发治疗基础编辑器的影响.

主要方法:

  • 关于AID的酶性质和细胞背景的最新研究的综述.
  • 与AID活动相关的DNA基质灵活性和染色质可访问性的分析.
  • 检查处理AID产生的病变的DNA修复途径.

主要成果:

  • 艾滋病优先针对灵活的DNA基质.
  • 在染色质循环域内,AID活动受到空间限制.
  • 不同的DNA修复因子差异地处理艾滋病引起的DNA损伤.
  • 由AID所造成的异常除会对细胞产生各种各样的后果.

结论:

  • 通过基质偏好,染色质环境和DNA修复途径,AID的活性受到严格的调节.
  • 了解这些监管机制是利用AID潜力的关键.
  • 对AID调节的洞察力可以指导基因治疗应用的基因编辑器的设计.