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相关概念视频

Chromatin Modification in iPS Cells01:32

Chromatin Modification in iPS Cells

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Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
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Nucleosome Remodeling02:54

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Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
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Epigenetic Regulation01:37

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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Histone Modification02:32

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The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
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相关实验视频

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Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
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在缺氧下进行表观遗传重塑.

Roxane Verdikt1, Bernard Thienpont2

  • 1Institute for Society and Genetics, University of California, Los Angeles, Los Angeles, CA, USA; Department of Human Genetics, KU Leuven, Leuven, Belgium; KU Leuven Institute for Single Cell Omics (LISCO), KU Leuven, Leuven, Belgium.

Seminars in cancer biology
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概括

缺氧,瘤中缺乏氧气,驱动癌症恶性和治疗耐药性. 表观遗传机制是癌细胞如何适应缺氧的关键,影响基因调节和代谢重编程以治疗开发.

关键词:
癌症项目 癌症项目表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.瘤缺氧是因为瘤缺氧.

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科学领域:

  • 在瘤学瘤学.
  • 分子生物学分子生物学
  • 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

  • 缺氧是固体瘤的一个常见特征.
  • 瘤缺氧促进癌症的进展,转移和对治疗的抵抗.
  • 表观遗传机制对于癌细胞适应低氧条件至关重要.

研究的目的:

  • 审查目前关于缺氧癌细胞中基因程序的表观遗传控制的文献.
  • 突出表观遗传改造的共同主题和特征,以应对缺氧.
  • 讨论这些发现对于开发新型治疗策略的相关性.

主要方法:

  • 对低氧癌细胞表观遗传调节研究的文献综述.
  • 分析常见的表观遗传修饰及其相关的基因表达变化.
  • 结合发现与已知的低氧敏感转录因子和代谢重编程.

主要成果:

  • 表观遗传机制对于感知氧气水平和适应慢性缺氧至关重要.
  • 涉及表观遗传调节,转录因子和代谢重编程的复杂网络控制着缺氧癌细胞程序.
  • 在表观遗传改造中常见的主题有助于瘤适应和在缺氧下进展.

结论:

  • 表观遗传控制是低氧癌细胞适应的一个核心机制.
  • 了解这些表观遗传变化为开发向癌症治疗提供了潜力.
  • 在低氧瘤中准表观遗传修饰可以克服治疗耐药性.