自噬
PI3K/AKT/mTOR通路
调节器
细胞生物学
TOR信号
生物
雷帕霉素的作用靶点
ULK1
RPTOR公司
主调节器
细胞生长
自噬相关蛋白13
营养感应
激酶
袋3
蛋白激酶A
信号转导
生物化学
转录因子
细胞凋亡
蛋白质磷酸化
基因
安普克
作者
Chang Hwa Jung,Seung Hyun Ro,Jing Cao,Neil Otto,Do‐Hyung Kim
出处
期刊:FEBS Letters
[Wiley]
日期:2010-01-18
卷期号:584 (7): 1287-1295
被引量:1805
标识
DOI:10.1016/j.febslet.2010.01.017
摘要
Nutrient starvation induces autophagy in eukaryotic cells through inhibition of TOR (target of rapamycin), an evolutionarily‐conserved protein kinase. TOR, as a central regulator of cell growth, plays a key role at the interface of the pathways that coordinately regulate the balance between cell growth and autophagy in response to nutritional status, growth factor and stress signals. Although TOR has been known as a key regulator of autophagy for more than a decade, the underlying regulatory mechanisms have not been clearly understood. This review discusses the recent advances in understanding of the mechanism by which TOR regulates autophagy with focus on mammalian TOR (mTOR) and its regulation of the autophagy machinery.
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