遗传 ›› 2022, Vol. 44 ›› Issue (1): 15-24.doi: 10.16288/j.yczz.21-329
收稿日期:
2021-09-13
修回日期:
2021-12-01
出版日期:
2022-01-20
发布日期:
2021-12-02
通讯作者:
许师明
E-mail:18428302536@163.com;xusm@e-mdic.cn
作者简介:
刘静,在读硕士研究生,专业方向:细胞生物学。E-mail: 基金资助:
Jing Liu(), Cong Yi, Shiming Xu()
Received:
2021-09-13
Revised:
2021-12-01
Online:
2022-01-20
Published:
2021-12-02
Contact:
Xu Shiming
E-mail:18428302536@163.com;xusm@e-mdic.cn
Supported by:
摘要:
自噬是一种依赖于液泡或溶酶体,从酵母到人类都高度保守的物质降解途径,其在维持细胞稳态过程中起重要作用。自噬功能的异常与人类多种重大疾病如神经退行性疾病、代谢性疾病及恶性肿瘤的发生发展密切相关。作为维持生物体内稳态平衡的重要生物学过程,细胞自噬的发生受到精密的调控。乙酰化修饰作为一种可逆的蛋白翻译后修饰(post-translational modification, PTM),在自噬的精密调控中发挥重要作用。本文主要对近年来乙酰化修饰在自噬调控中的相关研究进行了综述,以期为自噬领域的基础研究提供思路,同时也为研究人员探索自噬相关疾病的预防和治疗方法提供参考。
刘静, 易聪, 许师明. 蛋白质乙酰化修饰对自噬的调控作用[J]. 遗传, 2022, 44(1): 15-24.
Jing Liu, Cong Yi, Shiming Xu. The regulatory effect of protein acetylation modification on autophagy[J]. Hereditas(Beijing), 2022, 44(1): 15-24.
表1
自噬相关蛋白(ATG)的乙酰化对于自噬的调控"
蛋白 | 乙酰化位点 | 乙酰化酶/去乙酰化酶 | 对自噬的影响 | 相关文献 |
---|---|---|---|---|
ATG12 | — | p300/SIRT1 | ATG12乙酰化抑制自噬发生 | [ |
ATG9A | K359、K363 | —/SIRT1 | ATG9A的去乙酰不仅影响自噬体膜的形成,也充当内质网(ER)压力诱导自噬的传感器 | [ |
LC3 | K49、K51 | p300/SIRT1 | 去乙酰化的LC3转位到胞质内,参与自噬复合体的形成 | [ |
VPS34 | K29、K771 | p300/SIRT1 | p300依赖性乙酰化/去乙酰化是诱导VPS34激酶活化并参与自噬的关键 | [ |
ULK1 | K162、K606 | TIP60/— | ULK1的乙酰化是生长因子缺乏诱导的自噬所必需的 | [ |
ATG5 | — | p300/SIRT1 | ATG5乙酰化抑制自噬溶酶体的成熟 | [ |
ATG7 | — | p300/SIRT1 | ATG7乙酰化抑制自噬 | [ |
ATG3 | K19、K48 | Esa1/Rpd3 | ATG3的乙酰化通过控制ATG3和ATG8的相互作用以及ATG8的脂化来调节自噬 | [ |
Pacer | K483、K573 | TIP60/— | Pacer的乙酰化是自噬体成熟和细胞脂质代谢所必需的 | [ |
STX17 | K219、K223 | CBP/HDAC2 | STX17被募集到自噬体膜后,STX17的去乙酰化是其在自噬溶酶体融合中发挥作用的必不可少的步骤 | [ |
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