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NF-κB-dependent Signaling Pathway02:26

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Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
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Techniques to Induce and Quantify Cellular Senescence
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依赖NFκB动态的表观遗传变化调节炎性基因表达,并诱导细胞衰老.

Sho Tabata1, Keita Matsuda1, Shou Soeda1

  • 1Laboratory for Cell Systems, Institute for Protein Research, Osaka University, Suita, Japan.

The FEBS journal
|July 16, 2024
PubMed
概括

通过耗尽NFκB抑制剂α (IκBα) 来改变核因子 κB (NFκB) 信号动态,促进细胞衰老. 这种持续的NFκB活动驱动着炎症和衰老,影响基因表达和细胞周期进展.

关键词:
在 NFκBB 的情况下.在 SASP 找 SASP细胞衰老 细胞衰老炎症性衰老的炎症性衰老核动力学的核动力学

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科学领域:

  • 细胞生物学 细胞生物学
  • 分子生物学分子生物学
  • 衰老研究研究 衰老研究

背景情况:

  • 核因子 κB (NFκB) 信号在衰老中升级,并与慢性炎症有关.
  • 在细胞衰老中NFκB动态的确切作用仍然不清楚.

研究的目的:

  • 研究NFκB核动力学的变化如何影响细胞衰老.
  • 探索NFκB抑制剂α (IκBα) 在调节NFκB活性和衰老中的作用.

主要方法:

  • 在瘤亡因子α (TNFα) 存在时IκBα的耗尽,以改变NFκB的核动力学.
  • 评估NFκB-DNA结合,炎症基因表达和细胞周期进展.
  • 在复制性和氧化性压力下测量IκBα蛋白水平 in vitro.
  • 分析老老鼠心中的IκBα蛋白和NFκB-DNA结合.

主要成果:

  • 持续的NFκB活动,由IκBα耗尽引起,促进细胞衰老.
  • 随着持续的NFκB,观察到增强的炎症基因表达和细胞循环减缓.
  • 在复制性和氧化性压力下,IκBα蛋白减少.
  • 老鼠心脏显示IκBα降低,NFκB-DNA结合增加在与年龄相关的基因位置.

结论:

  • 改变NFκB核动力学,特别是由于IκBα减少而持续的活动,驱动细胞衰老.
  • 这个过程涉及NFκB依赖的表观遗传变化,增强炎症基因表达,促进衰老.
  • 核NFκB动态对于衰老和与年龄相关的炎症的进展至关重要.