生命的化学2023,Vol.43Issue(11) :1661-1669.DOI:10.13488/j.smhx.20230565

乙酰辅酶A与内质网乙酰化

Acetyl-CoA and acetylation of endoplasmic reticulum

张悦 王琪琳
生命的化学2023,Vol.43Issue(11) :1661-1669.DOI:10.13488/j.smhx.20230565

乙酰辅酶A与内质网乙酰化

Acetyl-CoA and acetylation of endoplasmic reticulum

张悦 1王琪琳1
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作者信息

  • 1. 聊城大学生命科学学院,聊城 252000
  • 折叠

摘要

乙酰辅酶A是细胞内物质和能量代谢的重要中间物,同时也是蛋白质乙酰化的乙酰基供体.蛋白质乙酰化包括Nα-乙酰化和Nε-乙酰化,由不同的酶进行催化.蛋白质乙酰化发生在多个亚细胞部位,如细胞基质、细胞核、线粒体和内质网腔等.不同细胞器和区室内乙酰辅酶A的波动可调控内质网蛋白质的乙酰化水平.本文从柠檬酸转运蛋白SLC25A1和SLC13A5、乙酰辅酶A转运蛋白AT-1以及乙酰转移酶ATase1和ATase2的功能出发,以相关人类疾病、内质网乙酰化失调小鼠模型和柠檬酸/乙酰辅酶A通量失调小鼠模型为背景进行分析,阐述了乙酰辅酶A和内质网乙酰化以及内质网乙酰化功能失调与退行性疾病之间的关系,旨在为靶向治疗相关疾病提供一定的策略.

Abstract

Acetyl-CoA is a key intermediate in substance and energy metabolism,and is also the acetyl group donor for protein acetylation.Protein acetylation includes Nα-acetylation and Nε-acetylation,which are catalyzed by different enzymes.Protein acetylation occurs in multiple subcellular organelles and compartments,such as cytosol,nucleus,mitochondria,endoplasmic reticulum lumen and so on.Studies have shown that fluctuations of acetyl-CoA availability in different organelles and compartments can regulate the levels of proteins acetylation in endoplasmic reticulum.Based on the functions of citrate transporters SLC25A1 and SLC13A5,acetyl-CoA transporters AT-1,and acetyltransferases ATase1 and ATase2,this paper analyzed the related human diseases and dysregulated mouse models relevant on endoplasmic reticulum acetylation or citrate/acetyl-CoA flux.Furthermore,this paper also summarized the relationship between acetyl-CoA and endoplasmic reticulum acetylation,and clarified that dysfunction of endoplasmic reticulum acetylation was closely related to the developmental and degenerative diseases,which could provide some certain strategies for treatment of the related diseases.

关键词

乙酰辅酶A/蛋白质乙酰化/内质网/AT-1/柠檬酸

Key words

acetyl-CoA/protein acetylation/endoplasmic reticulum/AT-1/citric acid

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基金项目

山东省自然科学基金(ZR2020MC066)

出版年

2023
生命的化学
中国生物化学与分子生物学会

生命的化学

CSTPCD
影响因子:0.404
ISSN:1000-1336
参考文献量56
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