自噬
生物
细胞生物学
安普克
磷酸化
葡萄糖稳态
钙信号传导
信号转导
平衡
激酶
胰高血糖素
钙
ULK1
钙调蛋白
生物化学
饥饿反应
蛋白激酶A
饥饿
内分泌学
内科学
酶
胰岛素
细胞凋亡
胰岛素抵抗
医学
激素
作者
Hai‐Bin Ruan,Yina Ma,Sara Sopeña Torres,Bichen Zhang,Colleen Feriod,Ryan Heck,Kevin Qian,Minnie Fu,Xiuqi Li,Michael H. Nathanson,Anton M. Bennett,Yongzhan Nie,Barbara E. Ehrlich,Xiaoyong Yang
出处
期刊:Genes & Development
[Cold Spring Harbor Laboratory Press]
日期:2017-08-15
卷期号:31 (16): 1655-1665
被引量:129
标识
DOI:10.1101/gad.305441.117
摘要
Starvation induces liver autophagy, which is thought to provide nutrients for use by other organs and thereby maintain whole-body homeostasis. Here we demonstrate that O-linked β-N-acetylglucosamine (O-GlcNAc) transferase (OGT) is required for glucagon-stimulated liver autophagy and metabolic adaptation to starvation. Genetic ablation of OGT in mouse livers reduces autophagic flux and the production of glucose and ketone bodies. Upon glucagon-induced calcium signaling, calcium/calmodulin-dependent kinase II (CaMKII) phosphorylates OGT, which in turn promotes O-GlcNAc modification and activation of Ulk proteins by potentiating AMPK-dependent phosphorylation. These findings uncover a signaling cascade by which starvation promotes autophagy through OGT phosphorylation and establish the importance of O-GlcNAc signaling in coupling liver autophagy to nutrient homeostasis.
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