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Epigenetic Regulation01:46

Epigenetic Regulation

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Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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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.
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Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
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Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
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Biochemical reactions are occurring constantly in cells, converting starting substances to different products, usually with the help of enzymes that speed the reactions. Without enzymes, it would take far too long for most reactions to occur to be useful to the cell!
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Guanine nucleotide-binding proteins (G-proteins), also known as GTPases, are a superfamily of proteins that regulate many cellular processes, such as cell signaling, vesicular transport, and the regulation of cell shape and motility. Mutation or dysfunction of these proteins can lead to disease. There are around 40,000 known G-proteins that can broadly be classified into two groups ‒  small G-proteins consisting of a single domain and large multi-domain G-proteins.
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相关实验视频

Updated: Jan 29, 2026

Analysis of Oxidative Stress in Zebrafish Embryos
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通过表观遗传调节p66shc介导的氧化应激途径诱导内皮功能障碍

Yunjun Xiao1, Junjie Xia1, Jinquan Cheng1

  • 1Shenzhen Key Laboratory of Molecular Epidemiology (Y.X., J.X., J.C., Y.Z., YK.), Shenzhen Center for Disease Control and Prevention, Guangdong, China.

Circulation
|February 19, 2019
PubMed
概括

通过表观遗传上调p66shc,导致动脉样硬化,增加的S- 腺homocysteine (SAH) 水平会损害内皮功能. 这项研究揭示了一种将SAH与内皮损伤联系起来的新机制.

关键词:
S-Adenosylhomocysteine 的使用情况细胞内膜遗传学甲基转移酶氧化应激

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相关实验视频

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科学领域:

  • 心血管研究
  • 分子生物学
  • 表观遗传学

背景情况:

  • 增加的S- 腺 homocysteine (SAH) 与心血管疾病和动脉样硬化有关.
  • 在内皮功能障碍中SAH的具体作用尚不清楚.

研究的目的:

  • 研究SAH在大动脉内皮功能障碍中的作用.
  • 阐明SAH引起的内皮损伤背后的分子机制.

主要方法:

  • 在使用SAHH抑制剂或shRNA的小鼠模型 (apoE-/-小鼠,SAHH+/-小鼠) 中,SAHH水平升高.
  • 评估了内皮功能,氧化的生物可用性和氧化应激.
  • 在小鼠大动脉和人类细胞中分析了表观遗传修饰,包括DNA甲基化和基因表达 (p66shc,DNMT1).
  • 人类研究与冠状动脉疾病患者的内皮功能和基因促进物甲基化相关联.

主要成果:

  • 抑制SAHH会增加血SAH水平,并影响内皮血管扩张和氧化的生物可用性.
  • 通过p66shc促进物的低甲基化,SAHH抑制诱导了反应性氧物种的产生和p66shc的表达.
  • 通过SAHH抑制抑制了DNA甲基转移酶1 (DNMT1) 的表达,其过度表达取消了p66shc上调.
  • 在人体中,较高的SAH水平与流媒体扩张的减少和氧化应激的增加相关.

结论:

  • 通过对p66shc介导的氧化应激通路的表观调节,SAHH抑制导致SAH升高和内皮功能障碍.
  • 这项研究提供了有关SAH导致动脉样硬化的内皮损伤机制的新见解.
  • 针对SAH相关的表观遗传修饰可能为心血管疾病提供治疗策略.