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细胞衰老中的ubiquitination和acetylation:机制,交叉声和治疗影响
Mengjiao Yu1, Jiaxin Liu1, Weiwei Shi2
1Institute for Applied Research in Public Health, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, China.
概括
由翻译后修饰 (PTMs) 驱动的细胞衰老会破坏组织平衡. 这篇评论详细介绍了ubiquitination和acetylation如何协调衰老,为抗衰老疗法提供了目标.
科学领域:
- 老年学是一门学科.
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 细胞衰老是衰老和与年龄相关的疾病的一个关键因素.
- 翻译后修饰 (PTMs) 关键调节衰老.
- 本综述侧重于衰老中的泛化和乙化.
研究的目的:
- 审查在细胞衰老中泛化和乙化的作用.
- 探索这些PTM的机制和后果.
- 讨论针对这些修改的治疗策略.
主要方法:
- 在衰老过程中对ubiquitination和acetylation的文献综述.
- 对涉及p53,p21,p16,自,DNA损伤反应和SASP的调节通路的分析.
- 检查ubiquitination和乙化之间的交叉关系.
- 目前药理干预措施的总结.
主要成果:
- 通过各种各样的ubiquitin链类型,ubiquitin化调节关键的衰老蛋白和通路.
- 乙化,由乙转移酶和脱乙酶调节,控制细胞循环,DNA修复,炎症和线粒体功能.
- 无处不在和乙化之间的相互作用形成了复杂的衰老网络.
- 对这些PTM的药理向显示出对抗衰老干预措施的希望.
结论:
- 乌比基化和乙化是关键的PTMs编排细胞衰老.
- 了解它们的交叉通话提供了对衰老网络的洞察.
- 针对这些修改,为与年龄有关的疾病提供了潜在的治疗策略.
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