
아미노산 결핍 상황에서 SIRT2는 ACSS2의 K271 잔기를 탈아세틸화하여 ACSS2의 유비퀴틴화와 분해를 유도함으로써 지방 생합성을 억제한다.


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De novo lipogenesis is associated with the development of human diseases such as cancer, diabetes, and obesity. At the core of lipogenesis lies acetyl coenzyme A (CoA), a metabolite that plays a crucial role in fatty acid synthesis. One of the pathways contributing to the production of cytosolic acetyl-CoA is mediated by acetyl-CoA synthetase 2 (ACSS2). Here, we reveal that when cells encounter nutrient stress, particularly a deficiency in amino acids, Sirtuin 2 (SIRT2) catalyzes the deacetylation of ACSS2 at the lysine residue K271. This results in K271 ubiquitination and subsequently proteasomal degradation of ACSS2. Substitution of K271 leads to decreased ubiquitination of ACSS2, increased ACSS2 protein level, and thus increased lipogenesis. Our study uncovers a mechanism that cells employ to efficiently manage lipogenesis during periods of nutrient stress.

### Competing Interest Statement

HL is a founder and consultant for Sedec Therapeutics

SIRT2-Mediated ACSS2 K271 Deacetylation Suppresses Lipogenesis Under Nutrient Stress

아미노산-결핍-상황에서-sirt2에-의한-acss2-k271-탈아세틸화가-지방-생합성을-억제한다


아미노산 결핍 상황에서 SIRT2에 의한 ACSS2 K271 탈아세틸화가 지방 생합성을 억제한다
